Nutrient chapter

Potassium

Nutrient element potassium; dietary intake and body balance are distinct from free potassium ions or a serum measurement.

128 recorded mechanisms · 41 availability situations · 1 preserved sources. Draft and verified records are labeled separately.

Read recorded mechanisms Open recursive mind map

The mechanisms

What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.

High-salt/low-potassium feeding increased renal NCC phosphorylation in mice.
Potassium → NCC phosphorylation source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Low K availability increases signaling for sodium/chloride reabsorption.
evidence_location
Results; dietary NCC immunoblots.
experimental_model
Diet manipulation
limitations
pNCC is an activity-associated proxy; this is not a universal dietary threshold.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
With little dietary potassium, the kidney increases a sodium-chloride transporter signal.
primary_references
[terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006
tissue_or_cell_type
Distal convoluted tubule
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 99–110
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Diet manipulation · source_derived_draft · unverified_draft
### renal-low-k-activates-ncc High-salt/low-potassium feeding increased renal NCC phosphorylation in mice. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: With little dietary potassium, the kidney increases a sodium-chloride transporter signal. organism: Mus musculus tissue_or_cell_type: Distal convoluted tubule experimental_model: Diet manipulation limitations: pNCC is an activity-associated proxy; this is not a universal dietary threshold. cross_nutrient: Low K availability increases signaling for sodium/chloride reabsorption. evidence_location: Results; dietary NCC immunoblots. [terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006
Complete structured claim and evidence
Low-potassium feeding on high salt reduced sodium excretion; NCC deletion blunted the blood-pressure response.
Thiazide-sensitive sodium-chloride cotransporter → Renal sodium reabsorption source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium restriction changes sodium handling through NCC.
evidence_location
Figure 2A-C.
experimental_model
Wild-type versus Slc12a3-null dietary study
limitations
Knockout tests pathway contribution, not exclusive control of pressure.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
Potassium scarcity can make sodium retention easier through NCC.
primary_references
[terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006
tissue_or_cell_type
Kidney
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 112–123
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Wild-type versus Slc12a3-null dietary study · source_derived_draft · unverified_draft
### renal-low-k-ncc-salt-retention Low-potassium feeding on high salt reduced sodium excretion; NCC deletion blunted the blood-pressure response. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium scarcity can make sodium retention easier through NCC. organism: Mus musculus tissue_or_cell_type: Kidney experimental_model: Wild-type versus Slc12a3-null dietary study limitations: Knockout tests pathway contribution, not exclusive control of pressure. cross_nutrient: Potassium restriction changes sodium handling through NCC. evidence_location: Figure 2A-C. [terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006
Complete structured claim and evidence
Low-K medium lowered intracellular chloride in HEK293 and mDCT cells; depolarizing Kir4.1 mutants increased it.
Potassium ion → Intracellular chloride concentration source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Extracellular K controls the intracellular chloride signal.
evidence_location
Figure 6A-B; Figure S5.
experimental_model
Cell culture and Kir4.1 mutant comparisons
limitations
HEK chloride and WNK expression differ from native DCT.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens; Mus musculus cell lines
plain_language
A change outside the cell can change chloride inside, connecting potassium sensing to salt transport.
primary_references
[terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006
tissue_or_cell_type
HEK293 and mDCT cells
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 125–136
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell culture and Kir4.1 mutant comparisons · source_derived_draft · unverified_draft
### renal-low-external-k-lowers-cell-chloride Low-K medium lowered intracellular chloride in HEK293 and mDCT cells; depolarizing Kir4.1 mutants increased it. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A change outside the cell can change chloride inside, connecting potassium sensing to salt transport. organism: Homo sapiens; Mus musculus cell lines tissue_or_cell_type: HEK293 and mDCT cells experimental_model: Cell culture and Kir4.1 mutant comparisons limitations: HEK chloride and WNK expression differ from native DCT. cross_nutrient: Extracellular K controls the intracellular chloride signal. evidence_location: Figure 6A-B; Figure S5. [terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006
Complete structured claim and evidence
Increasing chloride inhibited recombinant WNK4 phosphorylation of SPAK more strongly than WNK1/3 in matched assays.
Chloride ion → WNK lysine deficient protein kinase 4 source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Chloride concentration gates a kinase linking K sensing to Na transport.
evidence_location
Figure 3; equimolar chloride/gluconate kinase assay.
experimental_model
Purified kinase domains; SPAK substrate
limitations
Does not directly measure native DCT chloride or WNK4 autophosphorylation.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Recombinant proteins
plain_language
Chloride restrains WNK4, a kinase upstream of sodium-chloride transport.
primary_references
[terker-2016-wnk4-chloride] Unique chloride-sensing properties of WNK4 permit the distal nephron to modulate potassium homeostasis (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4814375/ DOI: 10.1038/ki.2015.289
tissue_or_cell_type
Cell-free assay
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 138–149
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified kinase domains; SPAK substrate · source_derived_draft · unverified_draft
### renal-chloride-inhibits-wnk4 Increasing chloride inhibited recombinant WNK4 phosphorylation of SPAK more strongly than WNK1/3 in matched assays. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Chloride restrains WNK4, a kinase upstream of sodium-chloride transport. organism: Recombinant proteins tissue_or_cell_type: Cell-free assay experimental_model: Purified kinase domains; SPAK substrate limitations: Does not directly measure native DCT chloride or WNK4 autophosphorylation. cross_nutrient: Chloride concentration gates a kinase linking K sensing to Na transport. evidence_location: Figure 3; equimolar chloride/gluconate kinase assay. [terker-2016-wnk4-chloride] Unique chloride-sensing properties of WNK4 permit the distal nephron to modulate potassium homeostasis (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4814375/ DOI: 10.1038/ki.2015.289
Complete structured claim and evidence
Catalytically active WNK4 phosphorylated and activated SPAK in biochemical assays.
WNK lysine deficient protein kinase 4 → STE20/SPS1-related proline/alanine-rich kinase source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
This kinase relay can regulate sodium/chloride transport downstream of K sensing.
evidence_location
Primary abstract; kinase-activity and substrate-phosphorylation experiments.
experimental_model
Recombinant kinase assay
limitations
Establishes biochemical capability; not dietary potassium regulation by itself.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Recombinant proteins
plain_language
WNK4 passes a phosphate signal to SPAK.
primary_references
[vitari-2005-wnk-spak-osr1] The WNK1 and WNK4 protein kinases that are mutated in Gordon's hypertension syndrome phosphorylate and activate SPAK and OSR1 protein kinases (2005). https://pubmed.ncbi.nlm.nih.gov/16083423/ DOI: 10.1042/BJ20051180
tissue_or_cell_type
Cell-free assay
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 151–162
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant kinase assay · source_derived_draft · unverified_draft
### renal-wnk4-activates-spak Catalytically active WNK4 phosphorylated and activated SPAK in biochemical assays. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: WNK4 passes a phosphate signal to SPAK. organism: Recombinant proteins tissue_or_cell_type: Cell-free assay experimental_model: Recombinant kinase assay limitations: Establishes biochemical capability; not dietary potassium regulation by itself. cross_nutrient: This kinase relay can regulate sodium/chloride transport downstream of K sensing. evidence_location: Primary abstract; kinase-activity and substrate-phosphorylation experiments. [vitari-2005-wnk-spak-osr1] The WNK1 and WNK4 protein kinases that are mutated in Gordon's hypertension syndrome phosphorylate and activate SPAK and OSR1 protein kinases (2005). https://pubmed.ncbi.nlm.nih.gov/16083423/ DOI: 10.1042/BJ20051180
Complete structured claim and evidence
SPAK phosphorylated human NCC at Thr46, Thr55 and Thr60; Thr60 mutation impaired chloride-depletion-induced NCC activation.
STE20/SPS1-related proline/alanine-rich kinase → Thiazide-sensitive sodium-chloride cotransporter source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Defines the sodium/chloride transporter step of the potassium switch.
evidence_location
Primary abstract; phosphosite mapping, docking and Thr60Ala assays.
experimental_model
Recombinant phosphosite mapping and cell mutants
limitations
The dietary K response was not tested in this experiment.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Human protein; HEK293/mpkDCT cells
plain_language
A kinase modifies the sodium-chloride transporter at regulatory sites.
primary_references
[richardson-2008-spak-osr1-ncc] Activation of the thiazide-sensitive Na+-Cl- cotransporter by the WNK-regulated kinases SPAK and OSR1 (2008). https://pubmed.ncbi.nlm.nih.gov/18270262/ DOI: 10.1242/jcs.025312
tissue_or_cell_type
Biochemical assay and cultured kidney-derived cells
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 164–175
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant phosphosite mapping and cell mutants · source_derived_draft · unverified_draft
### renal-stk39-phosphorylates-ncc SPAK phosphorylated human NCC at Thr46, Thr55 and Thr60; Thr60 mutation impaired chloride-depletion-induced NCC activation. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A kinase modifies the sodium-chloride transporter at regulatory sites. organism: Human protein; HEK293/mpkDCT cells tissue_or_cell_type: Biochemical assay and cultured kidney-derived cells experimental_model: Recombinant phosphosite mapping and cell mutants limitations: The dietary K response was not tested in this experiment. cross_nutrient: Defines the sodium/chloride transporter step of the potassium switch. evidence_location: Primary abstract; phosphosite mapping, docking and Thr60Ala assays. [richardson-2008-spak-osr1-ncc] Activation of the thiazide-sensitive Na+-Cl- cotransporter by the WNK-regulated kinases SPAK and OSR1 (2008). https://pubmed.ncbi.nlm.nih.gov/18270262/ DOI: 10.1242/jcs.025312
Complete structured claim and evidence
OSR1 phosphorylated human NCC at Thr46, Thr55 and Thr60; Thr60 mutation impaired chloride-depletion-induced NCC activation.
Oxidative stress responsive kinase 1 → Thiazide-sensitive sodium-chloride cotransporter source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Defines the sodium/chloride transporter step of the potassium switch.
evidence_location
Primary abstract; phosphosite mapping, docking and Thr60Ala assays.
experimental_model
Recombinant phosphosite mapping and cell mutants
limitations
The dietary K response was not tested in this experiment.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Human protein; HEK293/mpkDCT cells
plain_language
A kinase modifies the sodium-chloride transporter at regulatory sites.
primary_references
[richardson-2008-spak-osr1-ncc] Activation of the thiazide-sensitive Na+-Cl- cotransporter by the WNK-regulated kinases SPAK and OSR1 (2008). https://pubmed.ncbi.nlm.nih.gov/18270262/ DOI: 10.1242/jcs.025312
tissue_or_cell_type
Biochemical assay and cultured kidney-derived cells
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 177–188
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant phosphosite mapping and cell mutants · source_derived_draft · unverified_draft
### renal-oxsr1-phosphorylates-ncc OSR1 phosphorylated human NCC at Thr46, Thr55 and Thr60; Thr60 mutation impaired chloride-depletion-induced NCC activation. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A kinase modifies the sodium-chloride transporter at regulatory sites. organism: Human protein; HEK293/mpkDCT cells tissue_or_cell_type: Biochemical assay and cultured kidney-derived cells experimental_model: Recombinant phosphosite mapping and cell mutants limitations: The dietary K response was not tested in this experiment. cross_nutrient: Defines the sodium/chloride transporter step of the potassium switch. evidence_location: Primary abstract; phosphosite mapping, docking and Thr60Ala assays. [richardson-2008-spak-osr1-ncc] Activation of the thiazide-sensitive Na+-Cl- cotransporter by the WNK-regulated kinases SPAK and OSR1 (2008). https://pubmed.ncbi.nlm.nih.gov/18270262/ DOI: 10.1242/jcs.025312
Complete structured claim and evidence
Adult renal Kir4.1 deletion depolarized DCT cells and abolished their voltage response to plasma potassium.
Inward rectifier potassium channel Kir4.1 → DCT membrane potential source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
Potassium conductance is needed to regulate apical sodium/chloride transport.
evidence_location
Abstract and Discussion; DCT patch-clamp experiments.
experimental_model
Inducible adult kidney-specific Kcnj10 deletion
limitations
Genetic loss is not dietary deficiency; Kir5.1 participation was not directly deleted in this study.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
Without Kir4.1, DCT cells lose the electrical response used to sense potassium.
primary_references
[cuevas-2017-kir4-sensing] Potassium Sensing by Renal Distal Tubules Requires Kir4.1 (2017). https://pmc.ncbi.nlm.nih.gov/articles/PMC5461801/ DOI: 10.1681/ASN.2016090935
tissue_or_cell_type
DCT basolateral membrane
trigger_kind
machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 190–201
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible adult kidney-specific Kcnj10 deletion · source_derived_draft · unverified_draft
### renal-kir4-loss-disables-sensing Adult renal Kir4.1 deletion depolarized DCT cells and abolished their voltage response to plasma potassium. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Without Kir4.1, DCT cells lose the electrical response used to sense potassium. organism: Mus musculus tissue_or_cell_type: DCT basolateral membrane experimental_model: Inducible adult kidney-specific Kcnj10 deletion limitations: Genetic loss is not dietary deficiency; Kir5.1 participation was not directly deleted in this study. cross_nutrient: Potassium conductance is needed to regulate apical sodium/chloride transport. evidence_location: Abstract and Discussion; DCT patch-clamp experiments. [cuevas-2017-kir4-sensing] Potassium Sensing by Renal Distal Tubules Requires Kir4.1 (2017). https://pmc.ncbi.nlm.nih.gov/articles/PMC5461801/ DOI: 10.1681/ASN.2016090935
Complete structured claim and evidence
Kcnj16-null mice failed to change NCC abundance/phosphorylation with high- or low-K diets despite persistent Kir4.1 conductance.
Inward rectifier potassium channel Kir5.1 → Thiazide-sensitive sodium-chloride cotransporter source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
Defective K sensing prevents appropriate sodium/chloride transporter adjustment.
evidence_location
Results and primary abstract; dietary electrophysiology and NCC assays.
experimental_model
Kir5.1 knockout with high/low K diets
limitations
Kir4.1 homomer conductance increases; this differs from Kir4.1 deletion.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
The Kir5.1 partner allows this potassium channel system to adjust sodium transport when intake changes.
primary_references
[wang-2019-kir5-sensing] Deletion of Kir5.1 Impairs Renal Ability to Excrete Potassium during Increased Dietary Potassium Intake (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6683724/ DOI: 10.1681/ASN.2019010025
tissue_or_cell_type
DCT
trigger_kind
machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 203–214
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Kir5.1 knockout with high/low K diets · source_derived_draft · unverified_draft
### renal-kir5-loss-prevents-diet-ncc-response Kcnj16-null mice failed to change NCC abundance/phosphorylation with high- or low-K diets despite persistent Kir4.1 conductance. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The Kir5.1 partner allows this potassium channel system to adjust sodium transport when intake changes. organism: Mus musculus tissue_or_cell_type: DCT experimental_model: Kir5.1 knockout with high/low K diets limitations: Kir4.1 homomer conductance increases; this differs from Kir4.1 deletion. cross_nutrient: Defective K sensing prevents appropriate sodium/chloride transporter adjustment. evidence_location: Results and primary abstract; dietary electrophysiology and NCC assays. [wang-2019-kir5-sensing] Deletion of Kir5.1 Impairs Renal Ability to Excrete Potassium during Increased Dietary Potassium Intake (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6683724/ DOI: 10.1681/ASN.2019010025
Complete structured claim and evidence
In native mouse kidney preparations, low extracellular K increased NCC phosphorylation through chloride-conductance-dependent SPAK/OSR1 signaling.
Potassium ion → NCC phosphorylation source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
K concentration regulates sodium/chloride transport via chloride-sensitive signaling.
evidence_location
Abstract and Results; low chloride and DIDS comparisons.
experimental_model
Perfused kidney and kidney slices
limitations
Acute bath/perfusate manipulation is not whole-body potassium depletion.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
The low-potassium signal needs chloride movement to increase the transporter phosphate signal.
primary_references
[penton-2016-native-potassium-switch] Extracellular K+ rapidly controls NaCl cotransporter phosphorylation in the native distal convoluted tubule by Cl--dependent and independent mechanisms (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5088235/ DOI: 10.1113/JP272504
tissue_or_cell_type
Native DCT
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 216–227
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Perfused kidney and kidney slices · source_derived_draft · unverified_draft
### renal-native-low-k-requires-chloride-flux In native mouse kidney preparations, low extracellular K increased NCC phosphorylation through chloride-conductance-dependent SPAK/OSR1 signaling. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The low-potassium signal needs chloride movement to increase the transporter phosphate signal. organism: Mus musculus tissue_or_cell_type: Native DCT experimental_model: Perfused kidney and kidney slices limitations: Acute bath/perfusate manipulation is not whole-body potassium depletion. cross_nutrient: K concentration regulates sodium/chloride transport via chloride-sensitive signaling. evidence_location: Abstract and Results; low chloride and DIDS comparisons. [penton-2016-native-potassium-switch] Extracellular K+ rapidly controls NaCl cotransporter phosphorylation in the native distal convoluted tubule by Cl--dependent and independent mechanisms (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5088235/ DOI: 10.1113/JP272504
Complete structured claim and evidence
High-K-induced NCC dephosphorylation persisted during low extracellular chloride or chloride-channel blockade in mouse kidney preparations.
Potassium ion → NCC phosphorylation source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
High K can suppress the sodium/chloride transporter through additional signaling.
evidence_location
Primary abstract; low extracellular chloride and DIDS experiments.
experimental_model
Perfused kidney and kidney slices
limitations
Pharmacological/ionic tests do not prove every chloride-sensitive step is absent.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
The rapid high-potassium response can persist when tested chloride movements are disrupted.
primary_references
[penton-2016-native-potassium-switch] Extracellular K+ rapidly controls NaCl cotransporter phosphorylation in the native distal convoluted tubule by Cl--dependent and independent mechanisms (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5088235/ DOI: 10.1113/JP272504
tissue_or_cell_type
Native DCT
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 229–240
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Perfused kidney and kidney slices · source_derived_draft · unverified_draft
### renal-native-high-k-cl-independent-ncc-off High-K-induced NCC dephosphorylation persisted during low extracellular chloride or chloride-channel blockade in mouse kidney preparations. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The rapid high-potassium response can persist when tested chloride movements are disrupted. organism: Mus musculus tissue_or_cell_type: Native DCT experimental_model: Perfused kidney and kidney slices limitations: Pharmacological/ionic tests do not prove every chloride-sensitive step is absent. cross_nutrient: High K can suppress the sodium/chloride transporter through additional signaling. evidence_location: Primary abstract; low extracellular chloride and DIDS experiments. [penton-2016-native-potassium-switch] Extracellular K+ rapidly controls NaCl cotransporter phosphorylation in the native distal convoluted tubule by Cl--dependent and independent mechanisms (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5088235/ DOI: 10.1113/JP272504
Complete structured claim and evidence
Acute oral potassium failed to suppress NCC in mice carrying chloride-insensitive WNK4, unlike wild-type controls.
WNK4 L319F/L321F chloride-insensitive variant → NCC phosphorylation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
A chloride-sensing defect disrupts K control of sodium transport.
evidence_location
Primary abstract; acute gavage NCC comparison.
experimental_model
Wnk4 LLFF knockin; oral K gavage
limitations
Constitutive kinase activation and longer-term K responses must be distinguished.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
Making WNK4 insensitive to chloride blocks the rapid potassium response in this mouse model.
primary_references
[chen-2019-wnk4-sensor] WNK4 kinase is a physiological intracellular chloride sensor (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6410802/ DOI: 10.1073/pnas.1817220116
tissue_or_cell_type
Kidney DCT
trigger_kind
machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 242–253
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Wnk4 LLFF knockin; oral K gavage · source_derived_draft · unverified_draft
### renal-wnk4-chloride-mutant-blocks-acute-k-off Acute oral potassium failed to suppress NCC in mice carrying chloride-insensitive WNK4, unlike wild-type controls. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Making WNK4 insensitive to chloride blocks the rapid potassium response in this mouse model. organism: Mus musculus tissue_or_cell_type: Kidney DCT experimental_model: Wnk4 LLFF knockin; oral K gavage limitations: Constitutive kinase activation and longer-term K responses must be distinguished. cross_nutrient: A chloride-sensing defect disrupts K control of sodium transport. evidence_location: Primary abstract; acute gavage NCC comparison. [chen-2019-wnk4-sensor] WNK4 kinase is a physiological intracellular chloride sensor (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6410802/ DOI: 10.1073/pnas.1817220116
Complete structured claim and evidence
Chloride-insensitive WNK4 blocked high-K NCC dephosphorylation in HEK cells; the authors inferred that WNK4-SPAK inhibition is required for the rapid response.
WNK4 L319F/L321F chloride-insensitive variant → NCC phosphorylation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
Balance of kinase and phosphatase signaling controls Na/Cl transport responses to K.
evidence_location
Discussion; WNK4-LLFF HEK experiment and acute-versus-prolonged restriction comparison.
experimental_model
HEK mutant expression with complementary mouse/kidney-slice experiments
limitations
Inference about obligatory kinase shutdown is disputed; model and adaptation time matter.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens cell line; Mus musculus
plain_language
A strongly active kinase relay can keep NCC phosphorylated during an acute potassium challenge.
primary_references
[yang-2021-ncc-off-switch] Roles of WNK4 and SPAK in K+-mediated dephosphorylation of the NaCl cotransporter (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8174808/ DOI: 10.1152/ajprenal.00459.2020
tissue_or_cell_type
HEK cells and renal DCT
trigger_kind
machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 255–266
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HEK mutant expression with complementary mouse/kidney-slice experiments · source_derived_draft · unverified_draft
### renal-wnk4-spak-activation-opposes-acute-off Chloride-insensitive WNK4 blocked high-K NCC dephosphorylation in HEK cells; the authors inferred that WNK4-SPAK inhibition is required for the rapid response. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A strongly active kinase relay can keep NCC phosphorylated during an acute potassium challenge. organism: Homo sapiens cell line; Mus musculus tissue_or_cell_type: HEK cells and renal DCT experimental_model: HEK mutant expression with complementary mouse/kidney-slice experiments limitations: Inference about obligatory kinase shutdown is disputed; model and adaptation time matter. cross_nutrient: Balance of kinase and phosphatase signaling controls Na/Cl transport responses to K. evidence_location: Discussion; WNK4-LLFF HEK experiment and acute-versus-prolonged restriction comparison. [yang-2021-ncc-off-switch] Roles of WNK4 and SPAK in K+-mediated dephosphorylation of the NaCl cotransporter (2021). https://pmc.ncbi.nlm.nih.gov/articles/PMC8174808/ DOI: 10.1152/ajprenal.00459.2020
Complete structured claim and evidence
PP1A directly bound the NCC regulatory terminus and dephosphorylated NCC; high extracellular K enhanced their association in MDCKI-hNCC cells.
Protein phosphatase 1 catalytic subunit alpha → Thiazide-sensitive sodium-chloride cotransporter source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
K-dependent phosphatase engagement reduces the activation signal of the Na/Cl transporter.
evidence_location
Figure 6A-C.
experimental_model
Purified binding/phosphatase assays and MDCKI-hNCC cells
limitations
Binding/activity assays do not by themselves quantify sodium transport in humans.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Recombinant proteins; Canis lupus familiaris cell line expressing human NCC
plain_language
Potassium can increase contact between NCC and an enzyme that removes its phosphate signal.
primary_references
[grimm-2023-pp1a-ncc] Dietary potassium stimulates Ppp1Ca-Ppp1r1a dephosphorylation of kidney NaCl cotransporter and reduces blood pressure (2023). https://www.jci.org/articles/view/158498 DOI: 10.1172/JCI158498
tissue_or_cell_type
Cell-free and kidney-derived cells
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 268–279
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified binding/phosphatase assays and MDCKI-hNCC cells · source_derived_draft · unverified_draft
### renal-pp1a-dephosphorylates-ncc PP1A directly bound the NCC regulatory terminus and dephosphorylated NCC; high extracellular K enhanced their association in MDCKI-hNCC cells. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium can increase contact between NCC and an enzyme that removes its phosphate signal. organism: Recombinant proteins; Canis lupus familiaris cell line expressing human NCC tissue_or_cell_type: Cell-free and kidney-derived cells experimental_model: Purified binding/phosphatase assays and MDCKI-hNCC cells limitations: Binding/activity assays do not by themselves quantify sodium transport in humans. cross_nutrient: K-dependent phosphatase engagement reduces the activation signal of the Na/Cl transporter. evidence_location: Figure 6A-C. [grimm-2023-pp1a-ncc] Dietary potassium stimulates Ppp1Ca-Ppp1r1a dephosphorylation of kidney NaCl cotransporter and reduces blood pressure (2023). https://www.jci.org/articles/view/158498 DOI: 10.1172/JCI158498
Complete structured claim and evidence
After high-K dietary adaptation, DCT-specific constitutively active SPAK mice reduced NCC phosphorylation despite persistent kinase activation.
Potassium → NCC phosphorylation source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
Dietary K adjusts the balance controlling Na/Cl transporter activation.
evidence_location
Figure 1; Figures 4-5; Discussion.
experimental_model
Four-day dietary K loading in CA-SPAK mice
limitations
Response required higher plasma K than controls; not a general claim that kinase state is irrelevant.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
With adaptation, the phosphate-removing response can overcome a continuously active kinase.
primary_references
[grimm-2023-pp1a-ncc] Dietary potassium stimulates Ppp1Ca-Ppp1r1a dephosphorylation of kidney NaCl cotransporter and reduces blood pressure (2023). https://www.jci.org/articles/view/158498 DOI: 10.1172/JCI158498
tissue_or_cell_type
DCT
trigger_kind
machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 281–292
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-day dietary K loading in CA-SPAK mice · source_derived_draft · unverified_draft
### renal-k-adaptation-overcomes-active-spak After high-K dietary adaptation, DCT-specific constitutively active SPAK mice reduced NCC phosphorylation despite persistent kinase activation. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: With adaptation, the phosphate-removing response can overcome a continuously active kinase. organism: Mus musculus tissue_or_cell_type: DCT experimental_model: Four-day dietary K loading in CA-SPAK mice limitations: Response required higher plasma K than controls; not a general claim that kinase state is irrelevant. cross_nutrient: Dietary K adjusts the balance controlling Na/Cl transporter activation. evidence_location: Figure 1; Figures 4-5; Discussion. [grimm-2023-pp1a-ncc] Dietary potassium stimulates Ppp1Ca-Ppp1r1a dephosphorylation of kidney NaCl cotransporter and reduces blood pressure (2023). https://www.jci.org/articles/view/158498 DOI: 10.1172/JCI158498
Complete structured claim and evidence
Oral K rapidly dephosphorylated NCC in mice, including aldosterone-deficient animals.
Potassium → NCC phosphorylation source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
K loading suppresses a Na/Cl transporter before some hormonal adaptations.
evidence_location
Primary abstract; early NCC time course and aldosterone-deficient mice.
experimental_model
Gastric K load; aldosterone-deficient comparison
limitations
Early response differs from later ENaC activation; acute gavage is not a chronic diet.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
The earliest NCC response to potassium does not require a new aldosterone signal in this model.
primary_references
[sorensen-2013-oral-k-ncc] Rapid dephosphorylation of the renal sodium chloride cotransporter in response to oral potassium intake in mice (2013). https://pubmed.ncbi.nlm.nih.gov/23447069/ DOI: 10.1038/ki.2013.14
tissue_or_cell_type
Kidney DCT
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 294–305
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Gastric K load; aldosterone-deficient comparison · source_derived_draft · unverified_draft
### renal-oral-k-aldosterone-independent-ncc-off Oral K rapidly dephosphorylated NCC in mice, including aldosterone-deficient animals. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The earliest NCC response to potassium does not require a new aldosterone signal in this model. organism: Mus musculus tissue_or_cell_type: Kidney DCT experimental_model: Gastric K load; aldosterone-deficient comparison limitations: Early response differs from later ENaC activation; acute gavage is not a chronic diet. cross_nutrient: K loading suppresses a Na/Cl transporter before some hormonal adaptations. evidence_location: Primary abstract; early NCC time course and aldosterone-deficient mice. [sorensen-2013-oral-k-ncc] Rapid dephosphorylation of the renal sodium chloride cotransporter in response to oral potassium intake in mice (2013). https://pubmed.ncbi.nlm.nih.gov/23447069/ DOI: 10.1038/ki.2013.14
Complete structured claim and evidence
NCC-deficient mice showed markedly less sodium excretion after the acute oral K load than controls.
Thiazide-sensitive sodium-chloride cotransporter → Urinary sodium excretion source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
K loading can increase sodium excretion through NCC regulation.
evidence_location
Primary abstract; NCC-deficient natriuresis comparison.
experimental_model
NCC knockout and control K gavage
limitations
This does not establish that increased distal sodium delivery alone explains all kaliuresis.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
Turning NCC down contributes to the sodium loss caused by potassium loading.
primary_references
[sorensen-2013-oral-k-ncc] Rapid dephosphorylation of the renal sodium chloride cotransporter in response to oral potassium intake in mice (2013). https://pubmed.ncbi.nlm.nih.gov/23447069/ DOI: 10.1038/ki.2013.14
tissue_or_cell_type
Kidney
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 307–318
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · NCC knockout and control K gavage · source_derived_draft · unverified_draft
### renal-ncc-loss-blunts-k-natriuresis NCC-deficient mice showed markedly less sodium excretion after the acute oral K load than controls. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Turning NCC down contributes to the sodium loss caused by potassium loading. organism: Mus musculus tissue_or_cell_type: Kidney experimental_model: NCC knockout and control K gavage limitations: This does not establish that increased distal sodium delivery alone explains all kaliuresis. cross_nutrient: K loading can increase sodium excretion through NCC regulation. evidence_location: Primary abstract; NCC-deficient natriuresis comparison. [sorensen-2013-oral-k-ncc] Rapid dephosphorylation of the renal sodium chloride cotransporter in response to oral potassium intake in mice (2013). https://pubmed.ncbi.nlm.nih.gov/23447069/ DOI: 10.1038/ki.2013.14
Complete structured claim and evidence
After 48 hours of dietary K deficiency, rat CCD ROMK shifted from apical membrane toward endosomal/lysosomal locations.
Potassium → ROMK endocytosis source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_location
Abstract; early/late endosomal marker colocalization.
experimental_model
Dietary restriction; confocal localization
limitations
Localization supports internalization/degradation; microscopy does not directly measure secretion.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
The kidney removes potassium exit channels from the surface when potassium is scarce.
primary_references
[chu-2003-romk-endocytosis] Dietary potassium restriction stimulates endocytosis of ROMK channel in rat cortical collecting duct (2003). https://journals.physiology.org/doi/10.1152/ajprenal.00150.2003 DOI: 10.1152/ajprenal.00150.2003
tissue_or_cell_type
Cortical collecting duct
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 320–330
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary restriction; confocal localization · source_derived_draft · unverified_draft
### renal-low-k-romk-internalization After 48 hours of dietary K deficiency, rat CCD ROMK shifted from apical membrane toward endosomal/lysosomal locations. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney removes potassium exit channels from the surface when potassium is scarce. organism: Rattus norvegicus tissue_or_cell_type: Cortical collecting duct experimental_model: Dietary restriction; confocal localization limitations: Localization supports internalization/degradation; microscopy does not directly measure secretion. evidence_location: Abstract; early/late endosomal marker colocalization. [chu-2003-romk-endocytosis] Dietary potassium restriction stimulates endocytosis of ROMK channel in rat cortical collecting duct (2003). https://journals.physiology.org/doi/10.1152/ajprenal.00150.2003 DOI: 10.1152/ajprenal.00150.2003
Complete structured claim and evidence
ARH bound the ROMK internalization motif and promoted endocytosis in COS-7 cells; Arh deletion altered dietary regulation of renal ROMK.
Low-density lipoprotein receptor adaptor protein 1 → ROMK endocytosis source_derived_draftungraded
Experimental context and source evidence
evidence_location
Abstract; binding motif experiments and renal Arh-null comparison.
experimental_model
Binding, knockdown and Arh-null dietary experiments
limitations
Cell uptake mechanism and mouse dietary phenotype are complementary experiments.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Chlorocebus-derived COS-7 cells; Mus musculus
plain_language
An adaptor helps pull ROMK from the membrane and contributes to potassium-dependent channel adjustment.
primary_references
[fang-2009-arh-romk] The ARH adaptor protein regulates endocytosis of the ROMK potassium secretory channel in mouse kidney (2009). https://pmc.ncbi.nlm.nih.gov/articles/PMC2769171/ DOI: 10.1172/JCI37950
tissue_or_cell_type
Cell system and distal nephron
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 332–342
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Binding, knockdown and Arh-null dietary experiments · source_derived_draft · unverified_draft
### renal-arh-targets-romk-endocytosis ARH bound the ROMK internalization motif and promoted endocytosis in COS-7 cells; Arh deletion altered dietary regulation of renal ROMK. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An adaptor helps pull ROMK from the membrane and contributes to potassium-dependent channel adjustment. organism: Chlorocebus-derived COS-7 cells; Mus musculus tissue_or_cell_type: Cell system and distal nephron experimental_model: Binding, knockdown and Arh-null dietary experiments limitations: Cell uptake mechanism and mouse dietary phenotype are complementary experiments. evidence_location: Abstract; binding motif experiments and renal Arh-null comparison. [fang-2009-arh-romk] The ARH adaptor protein regulates endocytosis of the ROMK potassium secretory channel in mouse kidney (2009). https://pmc.ncbi.nlm.nih.gov/articles/PMC2769171/ DOI: 10.1172/JCI37950
Complete structured claim and evidence
Romk1-specific deletion blunted high-K-induced collecting-tubule ROMK surface recruitment and caused hyperkalemia during that challenge.
ROMK1 splice isoform → Apical ROMK channel abundance source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
evidence_location
Abstract; high-K channel-number and localization comparison.
experimental_model
Isoform-specific knockout; high-K diet
limitations
Baseline channel gating and NKCC2 phenotype were preserved; not equivalent to pan-ROMK deletion.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
This ROMK splice isoform helps increase potassium exit-channel availability when intake rises.
primary_references
[romk1-2016-isoform] Romk1 Knockout Mice Do Not Produce Bartter Phenotype but Exhibit Impaired K Excretion (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4777858/ DOI: 10.1074/jbc.M115.707877
tissue_or_cell_type
Collecting tubule
trigger_kind
machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 344–354
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isoform-specific knockout; high-K diet · source_derived_draft · unverified_draft
### renal-romk1-needed-high-k-adaptation Romk1-specific deletion blunted high-K-induced collecting-tubule ROMK surface recruitment and caused hyperkalemia during that challenge. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This ROMK splice isoform helps increase potassium exit-channel availability when intake rises. organism: Mus musculus tissue_or_cell_type: Collecting tubule experimental_model: Isoform-specific knockout; high-K diet limitations: Baseline channel gating and NKCC2 phenotype were preserved; not equivalent to pan-ROMK deletion. evidence_location: Abstract; high-K channel-number and localization comparison. [romk1-2016-isoform] Romk1 Knockout Mice Do Not Produce Bartter Phenotype but Exhibit Impaired K Excretion (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4777858/ DOI: 10.1074/jbc.M115.707877
Complete structured claim and evidence
Intercalated-cell BKalpha deletion abolished flow-stimulated K secretion in isolated mouse CCDs from both sexes.
Large-conductance calcium-activated potassium channel alpha subunit → Distal renal potassium secretion source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
A calcium-activated K channel connects tubular flow to K elimination.
evidence_location
Figure 5; sex context Figure 8.
experimental_model
Cell-specific knockout; high-K adaptation; microperfusion
limitations
Chronic blood K elevation occurred only in males; whole-animal urinary outputs showed compensation.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
Flow-dependent potassium secretion needs BK channels in intercalated cells.
primary_references
[carrisoza-2020-intercalated-bk] Intercalated cell BKalpha subunit is required for flow-induced K+ secretion (2020). https://insight.jci.org/articles/view/130553 DOI: 10.1172/jci.insight.130553
tissue_or_cell_type
CCD intercalated cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 356–367
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-specific knockout; high-K adaptation; microperfusion · source_derived_draft · unverified_draft
### renal-intercalated-bk-flow-secretion Intercalated-cell BKalpha deletion abolished flow-stimulated K secretion in isolated mouse CCDs from both sexes. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Flow-dependent potassium secretion needs BK channels in intercalated cells. organism: Mus musculus tissue_or_cell_type: CCD intercalated cells experimental_model: Cell-specific knockout; high-K adaptation; microperfusion limitations: Chronic blood K elevation occurred only in males; whole-animal urinary outputs showed compensation. cross_nutrient: A calcium-activated K channel connects tubular flow to K elimination. evidence_location: Figure 5; sex context Figure 8. [carrisoza-2020-intercalated-bk] Intercalated cell BKalpha subunit is required for flow-induced K+ secretion (2020). https://insight.jci.org/articles/view/130553 DOI: 10.1172/jci.insight.130553
Complete structured claim and evidence
Removing luminal Ca2+ or buffering intracellular Ca2+ suppressed flow-stimulated K secretion in microperfused rabbit CCDs.
Calcium ion → Distal renal potassium secretion source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Local calcium availability permits flow-stimulated potassium secretion.
evidence_location
Results; luminal Ca and intracellular buffering experiments.
experimental_model
Luminal Ca removal/BAPTA and flow challenge
limitations
Tests ion availability in vitro, not dietary calcium deficiency; the entry-channel identity was unresolved.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Oryctolagus cuniculus
plain_language
Calcium entry and signaling are required for this flow-driven potassium output.
primary_references
[liu-2007-calcium-flow] Ca2+ dependence of flow-stimulated K secretion in the mammalian cortical collecting duct (2007). https://journals.physiology.org/doi/10.1152/ajprenal.00057.2007 DOI: 10.1152/ajprenal.00057.2007
tissue_or_cell_type
Cortical collecting duct
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 369–380
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Luminal Ca removal/BAPTA and flow challenge · source_derived_draft · unverified_draft
### renal-calcium-entry-supports-flow-k-secretion Removing luminal Ca2+ or buffering intracellular Ca2+ suppressed flow-stimulated K secretion in microperfused rabbit CCDs. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium entry and signaling are required for this flow-driven potassium output. organism: Oryctolagus cuniculus tissue_or_cell_type: Cortical collecting duct experimental_model: Luminal Ca removal/BAPTA and flow challenge limitations: Tests ion availability in vitro, not dietary calcium deficiency; the entry-channel identity was unresolved. cross_nutrient: Local calcium availability permits flow-stimulated potassium secretion. evidence_location: Results; luminal Ca and intracellular buffering experiments. [liu-2007-calcium-flow] Ca2+ dependence of flow-stimulated K secretion in the mammalian cortical collecting duct (2007). https://journals.physiology.org/doi/10.1152/ajprenal.00057.2007 DOI: 10.1152/ajprenal.00057.2007
Complete structured claim and evidence
Benzamil inhibition of sodium absorption abolished the flow-stimulated increase in K secretion in rabbit CCDs.
Epithelial sodium channel → Distal renal potassium secretion source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Sodium transport through ENaC supports potassium secretion.
evidence_location
Figure 7 and associated Results.
experimental_model
Benzamil pretreatment and flow increase
limitations
Other species/segments can show ENaC-independent components; no universal requirement claimed.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Oryctolagus cuniculus
plain_language
Sodium entry through ENaC supports potassium secretion in this perfused segment.
primary_references
[liu-2007-calcium-flow] Ca2+ dependence of flow-stimulated K secretion in the mammalian cortical collecting duct (2007). https://journals.physiology.org/doi/10.1152/ajprenal.00057.2007 DOI: 10.1152/ajprenal.00057.2007
tissue_or_cell_type
Cortical collecting duct
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 382–393
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Benzamil pretreatment and flow increase · source_derived_draft · unverified_draft
### renal-enac-supports-rabbit-flow-k-secretion Benzamil inhibition of sodium absorption abolished the flow-stimulated increase in K secretion in rabbit CCDs. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sodium entry through ENaC supports potassium secretion in this perfused segment. organism: Oryctolagus cuniculus tissue_or_cell_type: Cortical collecting duct experimental_model: Benzamil pretreatment and flow increase limitations: Other species/segments can show ENaC-independent components; no universal requirement claimed. cross_nutrient: Sodium transport through ENaC supports potassium secretion. evidence_location: Figure 7 and associated Results. [liu-2007-calcium-flow] Ca2+ dependence of flow-stimulated K secretion in the mammalian cortical collecting duct (2007). https://journals.physiology.org/doi/10.1152/ajprenal.00057.2007 DOI: 10.1152/ajprenal.00057.2007
Complete structured claim and evidence
Nephron-wide MR deletion impaired apical ENaC orientation/cleavage and produced hyperkalemia with salt wasting in adult mice.
Mineralocorticoid receptor → ENaC proteolytic processing source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
Defective sodium-channel regulation compromises K balance.
evidence_location
Abstract; Results Figures 1 and 5.
experimental_model
Inducible renal MR deletion
limitations
NCC remained activatable by K restriction; receptor effects on NCC are not assumed to be direct.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
The mineralocorticoid receptor helps maintain the sodium-channel machinery needed for normal potassium balance.
primary_references
[terker-2016-mineralocorticoid] Direct and Indirect Mineralocorticoid Effects Determine Distal Salt Transport (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4978056/ DOI: 10.1681/ASN.2015070815
tissue_or_cell_type
Aldosterone-sensitive distal nephron
trigger_kind
machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 395–406
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible renal MR deletion · source_derived_draft · unverified_draft
### renal-mr-supports-enac-processing Nephron-wide MR deletion impaired apical ENaC orientation/cleavage and produced hyperkalemia with salt wasting in adult mice. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mineralocorticoid receptor helps maintain the sodium-channel machinery needed for normal potassium balance. organism: Mus musculus tissue_or_cell_type: Aldosterone-sensitive distal nephron experimental_model: Inducible renal MR deletion limitations: NCC remained activatable by K restriction; receptor effects on NCC are not assumed to be direct. cross_nutrient: Defective sodium-channel regulation compromises K balance. evidence_location: Abstract; Results Figures 1 and 5. [terker-2016-mineralocorticoid] Direct and Indirect Mineralocorticoid Effects Determine Distal Salt Transport (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4978056/ DOI: 10.1681/ASN.2015070815
Complete structured claim and evidence
Sgk1 phosphorylated Nedd4-2 at Ser444 and less strongly Ser338 in Xenopus constructs.
Serum and glucocorticoid-regulated kinase 1 → NEDD4-like E3 ubiquitin protein ligase source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
This biochemical sodium-channel pathway contributes to the machinery for K handling.
evidence_location
Figure 2.
experimental_model
Expression, kinase-dead and site-mutant experiments
limitations
Residue numbers are construct/species-specific; nutritional K sensing was not tested.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Xenopus laevis
plain_language
SGK1 modifies the protein that normally restrains sodium channels.
primary_references
[debonneville-2001-sgk-nedd4] Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression (2001). https://pubmed.ncbi.nlm.nih.gov/11742982/ DOI: 10.1093/emboj/20.24.7052
tissue_or_cell_type
Oocytes
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 408–419
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Expression, kinase-dead and site-mutant experiments · source_derived_draft · unverified_draft
### renal-sgk1-phosphorylates-nedd4l Sgk1 phosphorylated Nedd4-2 at Ser444 and less strongly Ser338 in Xenopus constructs. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: SGK1 modifies the protein that normally restrains sodium channels. organism: Xenopus laevis tissue_or_cell_type: Oocytes experimental_model: Expression, kinase-dead and site-mutant experiments limitations: Residue numbers are construct/species-specific; nutritional K sensing was not tested. cross_nutrient: This biochemical sodium-channel pathway contributes to the machinery for K handling. evidence_location: Figure 2. [debonneville-2001-sgk-nedd4] Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression (2001). https://pubmed.ncbi.nlm.nih.gov/11742982/ DOI: 10.1093/emboj/20.24.7052
Complete structured claim and evidence
SGK-dependent Nedd4-2 phosphorylation reduced its ENaC interaction and increased ENaC surface expression in oocytes.
SGK-phosphorylated NEDD4L → ENaC surface abundance source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Higher sodium-channel availability can support the secretory machinery used for K balance.
evidence_location
Figures 3-5; interaction and anti-FLAG surface-labeling experiments.
experimental_model
Oocyte binding, current and surface-labeling assays
limitations
Molecular sufficiency does not establish exclusive control in intact kidneys.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Xenopus laevis
plain_language
Phosphorylation weakens the sodium-channel removal signal, leaving more channels at the surface.
primary_references
[debonneville-2001-sgk-nedd4] Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression (2001). https://pubmed.ncbi.nlm.nih.gov/11742982/ DOI: 10.1093/emboj/20.24.7052
tissue_or_cell_type
Oocytes
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 421–432
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oocyte binding, current and surface-labeling assays · source_derived_draft · unverified_draft
### renal-phospho-nedd4l-releases-enac SGK-dependent Nedd4-2 phosphorylation reduced its ENaC interaction and increased ENaC surface expression in oocytes. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Phosphorylation weakens the sodium-channel removal signal, leaving more channels at the surface. organism: Xenopus laevis tissue_or_cell_type: Oocytes experimental_model: Oocyte binding, current and surface-labeling assays limitations: Molecular sufficiency does not establish exclusive control in intact kidneys. cross_nutrient: Higher sodium-channel availability can support the secretory machinery used for K balance. evidence_location: Figures 3-5; interaction and anti-FLAG surface-labeling experiments. [debonneville-2001-sgk-nedd4] Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression (2001). https://pubmed.ncbi.nlm.nih.gov/11742982/ DOI: 10.1093/emboj/20.24.7052
Complete structured claim and evidence
Renal Sgk1 deletion blunted the early increase in urinary K excretion on high-K feeding, with hyperkalemia and reduced ENaC processing.
Serum and glucocorticoid-regulated kinase 1 → Urinary potassium excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
Impaired ENaC sodium-channel adaptation accompanies defective K clearance.
evidence_location
Results Figure 2; two-day versus five-day dietary comparison.
experimental_model
Inducible tubular deletion; two-day high-K citrate diet
limitations
Excretion approached controls after longer adaptation; ROMK apical localization increased rather than decreased.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
Removing kidney SGK1 impairs the initial ability to clear a potassium load.
primary_references
[al-qusairi-2016-renal-sgk1] Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5005279/ DOI: 10.1152/ajprenal.00002.2016
tissue_or_cell_type
Kidney tubules
trigger_kind
machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 434–445
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible tubular deletion; two-day high-K citrate diet · source_derived_draft · unverified_draft
### renal-sgk1-loss-impairs-high-k-excretion Renal Sgk1 deletion blunted the early increase in urinary K excretion on high-K feeding, with hyperkalemia and reduced ENaC processing. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing kidney SGK1 impairs the initial ability to clear a potassium load. organism: Mus musculus tissue_or_cell_type: Kidney tubules experimental_model: Inducible tubular deletion; two-day high-K citrate diet limitations: Excretion approached controls after longer adaptation; ROMK apical localization increased rather than decreased. cross_nutrient: Impaired ENaC sodium-channel adaptation accompanies defective K clearance. evidence_location: Results Figure 2; two-day versus five-day dietary comparison. [al-qusairi-2016-renal-sgk1] Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5005279/ DOI: 10.1152/ajprenal.00002.2016
Complete structured claim and evidence
Removing luminal K reduced active transport current in rabbit cortical TAL; combining K removal with luminal barium nearly abolished it.
Potassium ion → Renal sodium reabsorption source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Luminal K availability supports coupled sodium/chloride reabsorption.
evidence_location
Primary abstract; ion-removal and conductance-blocking experiments.
experimental_model
Isolated perfused tubules; K removal and barium blockade
limitations
Electrical surrogate; the study predates molecular identification of NKCC2 and ROMK.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Oryctolagus cuniculus
plain_language
Recycled luminal potassium supports sodium and chloride uptake in the thick ascending limb.
primary_references
[greger-1981-luminal-k] Presence of luminal K+, a prerequisite for active NaCl transport in the cortical thick ascending limb of Henle's loop of rabbit kidney (1981). https://pubmed.ncbi.nlm.nih.gov/7322839/ DOI: 10.1007/BF00584588
tissue_or_cell_type
Cortical thick ascending limb
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 447–458
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated perfused tubules; K removal and barium blockade · source_derived_draft · unverified_draft
### renal-luminal-k-enables-tal-salt-transport Removing luminal K reduced active transport current in rabbit cortical TAL; combining K removal with luminal barium nearly abolished it. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Recycled luminal potassium supports sodium and chloride uptake in the thick ascending limb. organism: Oryctolagus cuniculus tissue_or_cell_type: Cortical thick ascending limb experimental_model: Isolated perfused tubules; K removal and barium blockade limitations: Electrical surrogate; the study predates molecular identification of NKCC2 and ROMK. cross_nutrient: Luminal K availability supports coupled sodium/chloride reabsorption. evidence_location: Primary abstract; ion-removal and conductance-blocking experiments. [greger-1981-luminal-k] Presence of luminal K+, a prerequisite for active NaCl transport in the cortical thick ascending limb of Henle's loop of rabbit kidney (1981). https://pubmed.ncbi.nlm.nih.gov/7322839/ DOI: 10.1007/BF00584588
Complete structured claim and evidence
Potassium-containing meals produced more renal K excretion than K-free meals plus intravenous KCl despite matched plasma K profiles in rats.
Potassium → Urinary potassium excretion source_derived_draftungraded
Experimental context and source evidence
evidence_location
Study 1 and primary abstract.
experimental_model
Meal comparison with plasma-profile-matched KCl infusion
limitations
The responsible sensor/factor was unidentified; matching sampled plasma does not exclude every local signal.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
The meal-associated signal adds to the effect of potassium measured in blood.
primary_references
[oh-2011-gut-k] Gut sensing of dietary K+ intake increases renal K+ excretion (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3154709/ DOI: 10.1152/ajpregu.00095.2011
tissue_or_cell_type
Gastrointestinal-renal axis
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 460–470
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Meal comparison with plasma-profile-matched KCl infusion · source_derived_draft · unverified_draft
### renal-rat-meal-k-excretion-beyond-plasma Potassium-containing meals produced more renal K excretion than K-free meals plus intravenous KCl despite matched plasma K profiles in rats. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The meal-associated signal adds to the effect of potassium measured in blood. organism: Rattus norvegicus tissue_or_cell_type: Gastrointestinal-renal axis experimental_model: Meal comparison with plasma-profile-matched KCl infusion limitations: The responsible sensor/factor was unidentified; matching sampled plasma does not exclude every local signal. evidence_location: Study 1 and primary abstract. [oh-2011-gut-k] Gut sensing of dietary K+ intake increases renal K+ excretion (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3154709/ DOI: 10.1152/ajpregu.00095.2011
Complete structured claim and evidence
A potassium-containing meal increased K excretion without a detected serum K rise in the human study; the response persisted with eplerenone.
Potassium → Urinary potassium excretion source_derived_draftungraded
Experimental context and source evidence
evidence_location
Primary abstract; meal-plus-K and eplerenone comparisons.
experimental_model
Controlled meal challenges and MR-blockade comparison; 32 participants
limitations
Low-sodium controlled background; no gut receptor identified and complete aldosterone independence is an inference.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
People can increase potassium excretion after a meal before a measurable blood rise.
primary_references
[preston-2015-gut-human] Evidence for a gastrointestinal-renal kaliuretic signaling axis in humans (2015). https://pubmed.ncbi.nlm.nih.gov/26308672/ DOI: 10.1038/ki.2015.243
tissue_or_cell_type
Gastrointestinal-renal axis
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 472–482
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled meal challenges and MR-blockade comparison; 32 participants · source_derived_draft · unverified_draft
### renal-human-meal-k-excretion-without-serum-rise A potassium-containing meal increased K excretion without a detected serum K rise in the human study; the response persisted with eplerenone. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: People can increase potassium excretion after a meal before a measurable blood rise. organism: Homo sapiens tissue_or_cell_type: Gastrointestinal-renal axis experimental_model: Controlled meal challenges and MR-blockade comparison; 32 participants limitations: Low-sodium controlled background; no gut receptor identified and complete aldosterone independence is an inference. evidence_location: Primary abstract; meal-plus-K and eplerenone comparisons. [preston-2015-gut-human] Evidence for a gastrointestinal-renal kaliuretic signaling axis in humans (2015). https://pubmed.ncbi.nlm.nih.gov/26308672/ DOI: 10.1038/ki.2015.243
Complete structured claim and evidence
Potassium-depleted MDCT cells showed reduced Mg2+ uptake in a magnesium-recovery assay.
Intracellular potassium content → Cellular magnesium influx source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Cellular K depletion decreases magnesium entry in this DCT model.
evidence_location
Primary abstract; potassium-depleted-cell Mg uptake comparison.
experimental_model
Cultured MDCT potassium depletion; fluorescence Mg-recovery assay
limitations
Intracellular depletion is distinct from low extracellular K alone; TRPM6 was not identified.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus cell line
plain_language
Depleting cellular potassium made it harder for these kidney cells to take up magnesium.
primary_references
[dai-1997-k-mg] Cellular mechanisms of chlorothiazide and cellular potassium depletion on Mg2+ uptake in mouse distal convoluted tubule cells (1997). https://pubmed.ncbi.nlm.nih.gov/9083264/ DOI: 10.1038/ki.1997.141
tissue_or_cell_type
Distal convoluted tubule cell model
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 484–495
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cultured MDCT potassium depletion; fluorescence Mg-recovery assay · source_derived_draft · unverified_draft
### renal-cellular-k-depletion-lowers-mg-influx Potassium-depleted MDCT cells showed reduced Mg2+ uptake in a magnesium-recovery assay. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Depleting cellular potassium made it harder for these kidney cells to take up magnesium. organism: Mus musculus cell line tissue_or_cell_type: Distal convoluted tubule cell model experimental_model: Cultured MDCT potassium depletion; fluorescence Mg-recovery assay limitations: Intracellular depletion is distinct from low extracellular K alone; TRPM6 was not identified. cross_nutrient: Cellular K depletion decreases magnesium entry in this DCT model. evidence_location: Primary abstract; potassium-depleted-cell Mg uptake comparison. [dai-1997-k-mg] Cellular mechanisms of chlorothiazide and cellular potassium depletion on Mg2+ uptake in mouse distal convoluted tubule cells (1997). https://pubmed.ncbi.nlm.nih.gov/9083264/ DOI: 10.1038/ki.1997.141
Complete structured claim and evidence
Thiocyanate-induced hyperpolarization restored Mg2+ uptake in potassium-depleted MDCT cells.
DCT membrane potential → Cellular magnesium influx source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
The K-depletion effect on Mg entry is partly recoverable by membrane polarization.
evidence_location
Primary abstract; SCN- rescue experiment.
experimental_model
SCN- voltage manipulation after cell K depletion
limitations
Supports partial voltage mediation; does not establish an in vivo repletion strategy.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus cell line
plain_language
Restoring the electrical driving force helped magnesium enter despite prior potassium depletion.
primary_references
[dai-1997-k-mg] Cellular mechanisms of chlorothiazide and cellular potassium depletion on Mg2+ uptake in mouse distal convoluted tubule cells (1997). https://pubmed.ncbi.nlm.nih.gov/9083264/ DOI: 10.1038/ki.1997.141
tissue_or_cell_type
Distal convoluted tubule cell model
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 497–508
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SCN- voltage manipulation after cell K depletion · source_derived_draft · unverified_draft
### renal-hyperpolarization-rescues-mg-after-k-depletion Thiocyanate-induced hyperpolarization restored Mg2+ uptake in potassium-depleted MDCT cells. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Restoring the electrical driving force helped magnesium enter despite prior potassium depletion. organism: Mus musculus cell line tissue_or_cell_type: Distal convoluted tubule cell model experimental_model: SCN- voltage manipulation after cell K depletion limitations: Supports partial voltage mediation; does not establish an in vivo repletion strategy. cross_nutrient: The K-depletion effect on Mg entry is partly recoverable by membrane polarization. evidence_location: Primary abstract; SCN- rescue experiment. [dai-1997-k-mg] Cellular mechanisms of chlorothiazide and cellular potassium depletion on Mg2+ uptake in mouse distal convoluted tubule cells (1997). https://pubmed.ncbi.nlm.nih.gov/9083264/ DOI: 10.1038/ki.1997.141
Complete structured claim and evidence
Low versus high dietary K increased calcium excretion in both salt-sensitive and salt-resistant Dahl rats on high NaCl.
Potassium → Urinary calcium excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Low K increases urinary calcium output under the tested sodium background.
evidence_location
Primary abstract; final-week balance results.
experimental_model
Four-week 0.2% versus 4% K diet; both 8% NaCl
limitations
Weanling males; unusual salt/mineral diets; causal transport site and BP mediation unproven.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
In this high-salt setting, lower potassium intake increased calcium loss in urine.
primary_references
[wu-1995-k-calcium] Potassium depletion and salt-sensitive hypertension in Dahl rats: effect on calcium, magnesium, and phosphate excretions (1995). https://pubmed.ncbi.nlm.nih.gov/7581265/ DOI: 10.3109/10641969509033647
tissue_or_cell_type
Kidney/urine
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 510–521
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-week 0.2% versus 4% K diet; both 8% NaCl · source_derived_draft · unverified_draft
### renal-low-k-increases-calcium-loss-high-salt Low versus high dietary K increased calcium excretion in both salt-sensitive and salt-resistant Dahl rats on high NaCl. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this high-salt setting, lower potassium intake increased calcium loss in urine. organism: Rattus norvegicus tissue_or_cell_type: Kidney/urine experimental_model: Four-week 0.2% versus 4% K diet; both 8% NaCl limitations: Weanling males; unusual salt/mineral diets; causal transport site and BP mediation unproven. cross_nutrient: Low K increases urinary calcium output under the tested sodium background. evidence_location: Primary abstract; final-week balance results. [wu-1995-k-calcium] Potassium depletion and salt-sensitive hypertension in Dahl rats: effect on calcium, magnesium, and phosphate excretions (1995). https://pubmed.ncbi.nlm.nih.gov/7581265/ DOI: 10.3109/10641969509033647
Complete structured claim and evidence
K-depleted rats preferentially retained K over Rb, especially when distal buffer delivery increased and residual secretion was inhibited.
Potassium → Renal potassium reabsorption source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
evidence_location
Primary abstract; K/Rb comparisons with buffer and secretion manipulation.
experimental_model
Clearance studies with amiloride and buffer-delivery manipulation
limitations
Clearance evidence does not identify the H,K-ATPase isoform or directly localize all transport.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
The depleted kidney can increase potassium recovery; rubidium does not track it perfectly.
primary_references
[1992-k-reabsorption] Effect of K depletion on renal K and Rb excretion: evidence for activation of K reabsorption (1992). https://pubmed.ncbi.nlm.nih.gov/1405312/ DOI: 10.1038/ki.1992.286
tissue_or_cell_type
Kidney; distal absorptive pathway inferred
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 523–533
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Clearance studies with amiloride and buffer-delivery manipulation · source_derived_draft · unverified_draft
### renal-k-depletion-activates-reabsorption K-depleted rats preferentially retained K over Rb, especially when distal buffer delivery increased and residual secretion was inhibited. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The depleted kidney can increase potassium recovery; rubidium does not track it perfectly. organism: Rattus norvegicus tissue_or_cell_type: Kidney; distal absorptive pathway inferred experimental_model: Clearance studies with amiloride and buffer-delivery manipulation limitations: Clearance evidence does not identify the H,K-ATPase isoform or directly localize all transport. evidence_location: Primary abstract; K/Rb comparisons with buffer and secretion manipulation. [1992-k-reabsorption] Effect of K depletion on renal K and Rb excretion: evidence for activation of K reabsorption (1992). https://pubmed.ncbi.nlm.nih.gov/1405312/ DOI: 10.1038/ki.1992.286
Complete structured claim and evidence
Supplementary KCl lowered total and phosphorylated NCC in urinary extracellular vesicles versus placebo in a randomized crossover study.
Potassium chloride → Urinary extracellular-vesicle NCC abundance source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
cross_nutrient
Human biomarker evidence links increased KCl intake to altered NaCl-transporter regulation.
evidence_location
Primary abstract; randomized crossover uEV immunoblots.
experimental_model
Five-day crossover phases; 18 analyzed healthy participants; controlled high-Na/low-K diet
limitations
Vesicle cargo is an indirect renal readout; no dietary recommendation or direct transport-flux inference.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
A human urine marker of the sodium-chloride transporter fell when potassium intake increased.
primary_references
[wu-2023-human-ncc] Randomized Trial on the Effect of Oral Potassium Chloride Supplementation on the Thiazide-Sensitive Sodium Chloride Cotransporter in Healthy Adults (2023). https://pmc.ncbi.nlm.nih.gov/articles/PMC10239795/ DOI: 10.1016/j.ekir.2023.03.011
tissue_or_cell_type
Urinary extracellular vesicles
trigger_kind
biomarker_context Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 535–546
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five-day crossover phases; 18 analyzed healthy participants; controlled high-Na/low-K diet · source_derived_draft · unverified_draft
### renal-human-kcl-lowers-uev-ncc Supplementary KCl lowered total and phosphorylated NCC in urinary extracellular vesicles versus placebo in a randomized crossover study. Condition category: biomarker_context nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A human urine marker of the sodium-chloride transporter fell when potassium intake increased. organism: Homo sapiens tissue_or_cell_type: Urinary extracellular vesicles experimental_model: Five-day crossover phases; 18 analyzed healthy participants; controlled high-Na/low-K diet limitations: Vesicle cargo is an indirect renal readout; no dietary recommendation or direct transport-flux inference. cross_nutrient: Human biomarker evidence links increased KCl intake to altered NaCl-transporter regulation. evidence_location: Primary abstract; randomized crossover uEV immunoblots. [wu-2023-human-ncc] Randomized Trial on the Effect of Oral Potassium Chloride Supplementation on the Thiazide-Sensitive Sodium Chloride Cotransporter in Healthy Adults (2023). https://pmc.ncbi.nlm.nih.gov/articles/PMC10239795/ DOI: 10.1016/j.ekir.2023.03.011
Complete structured claim and evidence
Cloned renal NKCC2 supported bumetanide-sensitive sodium-potassium-chloride cotransport in oocytes, distinct from NCC potassium-independent NaCl transport.
Sodium-potassium-chloride cotransporter 2 → NKCC2-mediated ion influx source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Potassium is a transported participant in this sodium/chloride entry mechanism.
evidence_location
Primary abstract; functional oocyte characterization.
experimental_model
Cloned renal cotransporter expression
limitations
Transport identity, not a dietary deficiency threshold; individual splice variants are not generalized.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mammalian proteins in Xenopus laevis oocytes
plain_language
NKCC2 moves potassium together with sodium and chloride; the related NCC transporter does not require potassium as cargo.
primary_references
[gamba-1994-nkcc2] Molecular cloning, primary structure, and characterization of two members of the mammalian electroneutral sodium-(potassium)-chloride cotransporter family expressed in kidney (1994). https://www.sciencedirect.com/science/article/pii/S0021925817324997 DOI: 10.1016/S0021-9258(17)32499-7
tissue_or_cell_type
Heterologous cell membrane
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 548–559
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cloned renal cotransporter expression · source_derived_draft · unverified_draft
### renal-nkcc2-couples-potassium-to-salt-influx Cloned renal NKCC2 supported bumetanide-sensitive sodium-potassium-chloride cotransport in oocytes, distinct from NCC potassium-independent NaCl transport. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: NKCC2 moves potassium together with sodium and chloride; the related NCC transporter does not require potassium as cargo. organism: Mammalian proteins in Xenopus laevis oocytes tissue_or_cell_type: Heterologous cell membrane experimental_model: Cloned renal cotransporter expression limitations: Transport identity, not a dietary deficiency threshold; individual splice variants are not generalized. cross_nutrient: Potassium is a transported participant in this sodium/chloride entry mechanism. evidence_location: Primary abstract; functional oocyte characterization. [gamba-1994-nkcc2] Molecular cloning, primary structure, and characterization of two members of the mammalian electroneutral sodium-(potassium)-chloride cotransporter family expressed in kidney (1994). https://www.sciencedirect.com/science/article/pii/S0021925817324997 DOI: 10.1016/S0021-9258(17)32499-7
Complete structured claim and evidence
Romk-null mice had reduced, but persisting, TAL NaCl absorption by micropuncture; the companion study demonstrated loss of native apical small-conductance K channels.
Renal outer medullary potassium channel / KCNJ1 → Renal sodium reabsorption source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
Loss of potassium-channel machinery impairs sodium/chloride recovery.
evidence_location
Lorenz primary abstract: micropuncture; Lu Results: TAL patch-clamp.
experimental_model
Pan-Romk deletion; micropuncture and companion patch-clamp studies
limitations
Hydronephrosis, developmental disease and compensatory transport complicate whole-kidney endpoints.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
ROMK-mediated potassium recycling supports loop salt recovery, while residual salt transport survives its deletion.
primary_references
[lorenz-2002-romk-tal] Impaired renal NaCl absorption in mice lacking the ROMK potassium channel, a model for type II Bartter's syndrome (2002). https://pubmed.ncbi.nlm.nih.gov/12122007/ DOI: 10.1074/jbc.M205627200 [lu-2002-romk-null] Absence of small conductance K+ channel (SK) activity in apical membranes of thick ascending limb and cortical collecting duct in ROMK (Bartter's) knockout mice (2002). https://pmc.ncbi.nlm.nih.gov/articles/PMC4426997/ DOI: 10.1074/jbc.M206644200
tissue_or_cell_type
Thick ascending limb
trigger_kind
machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 561–573
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pan-Romk deletion; micropuncture and companion patch-clamp studies · source_derived_draft · unverified_draft
### renal-romk-supports-tal-salt-reabsorption Romk-null mice had reduced, but persisting, TAL NaCl absorption by micropuncture; the companion study demonstrated loss of native apical small-conductance K channels. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: ROMK-mediated potassium recycling supports loop salt recovery, while residual salt transport survives its deletion. organism: Mus musculus tissue_or_cell_type: Thick ascending limb experimental_model: Pan-Romk deletion; micropuncture and companion patch-clamp studies limitations: Hydronephrosis, developmental disease and compensatory transport complicate whole-kidney endpoints. cross_nutrient: Loss of potassium-channel machinery impairs sodium/chloride recovery. evidence_location: Lorenz primary abstract: micropuncture; Lu Results: TAL patch-clamp. [lorenz-2002-romk-tal] Impaired renal NaCl absorption in mice lacking the ROMK potassium channel, a model for type II Bartter's syndrome (2002). https://pubmed.ncbi.nlm.nih.gov/12122007/ DOI: 10.1074/jbc.M205627200 [lu-2002-romk-null] Absence of small conductance K+ channel (SK) activity in apical membranes of thick ascending limb and cortical collecting duct in ROMK (Bartter's) knockout mice (2002). https://pmc.ncbi.nlm.nih.gov/articles/PMC4426997/ DOI: 10.1074/jbc.M206644200
Complete structured claim and evidence
External potassium supported ouabain-sensitive ATP hydrolysis when erythrocyte ghosts contained sodium, ATP and magnesium.
Potassium ion → Sodium-potassium ATPase complexes source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Potassium transport depends jointly on sodium and magnesium-supported ATP chemistry.
experimental_model
Resealed human erythrocyte ghosts; sided ion substitutions.
limitations
Sided activation adds to existing catalog flux/phosphorylation records; MgATP-only binding is not asserted.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Human
plain_language
Potassium outside and sodium inside activate complementary sides of the pump.
primary_references
[garrahan-1967-pump] The stoicheiometry of the sodium pump (1967). https://pmc.ncbi.nlm.nih.gov/articles/PMC1365482/ DOI: 10.1113/jphysiol.1967.sp008297
tissue_or_cell_type
Erythrocyte membrane
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 575–585
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Resealed human erythrocyte ghosts; sided ion substitutions. · source_derived_draft · unverified_draft
### k-pump-extracellular-activation External potassium supported ouabain-sensitive ATP hydrolysis when erythrocyte ghosts contained sodium, ATP and magnesium. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium outside and sodium inside activate complementary sides of the pump. organism: Human tissue_or_cell_type: Erythrocyte membrane experimental_model: Resealed human erythrocyte ghosts; sided ion substitutions. limitations: Sided activation adds to existing catalog flux/phosphorylation records; MgATP-only binding is not asserted. cross_nutrient: Potassium transport depends jointly on sodium and magnesium-supported ATP chemistry. [garrahan-1967-pump] The stoicheiometry of the sodium pump (1967). https://pmc.ncbi.nlm.nih.gov/articles/PMC1365482/ DOI: 10.1113/jphysiol.1967.sp008297
Complete structured claim and evidence
Ouabain-sensitive extrusion was approximately three sodium ions per ATP hydrolyzed in resealed erythrocyte ghosts.
Sodium-potassium ATPase complexes → Sodium-pump-mediated sodium efflux source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Sodium export couples to potassium-supported pump cycling and magnesium-dependent energy use.
experimental_model
Radiotracer sodium and ATP-hydrolysis assay.
limitations
This measurement does not itself establish an exact two-potassium ratio.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Human
plain_language
ATP consumption pays for sodium extrusion while potassium is available externally.
primary_references
[garrahan-1967-pump] The stoicheiometry of the sodium pump (1967). https://pmc.ncbi.nlm.nih.gov/articles/PMC1365482/ DOI: 10.1113/jphysiol.1967.sp008297
tissue_or_cell_type
Erythrocyte membrane
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 587–597
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiotracer sodium and ATP-hydrolysis assay. · source_derived_draft · unverified_draft
### k-pump-sodium-atp-coupling Ouabain-sensitive extrusion was approximately three sodium ions per ATP hydrolyzed in resealed erythrocyte ghosts. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: ATP consumption pays for sodium extrusion while potassium is available externally. organism: Human tissue_or_cell_type: Erythrocyte membrane experimental_model: Radiotracer sodium and ATP-hydrolysis assay. limitations: This measurement does not itself establish an exact two-potassium ratio. cross_nutrient: Sodium export couples to potassium-supported pump cycling and magnesium-dependent energy use. [garrahan-1967-pump] The stoicheiometry of the sodium pump (1967). https://pmc.ncbi.nlm.nih.gov/articles/PMC1365482/ DOI: 10.1113/jphysiol.1967.sp008297
Complete structured claim and evidence
The pig pump structure resolved two occluded rubidium ions at potassium transport sites in its alpha subunit.
Sodium-potassium ATPase complexes → Rubidium ion source_derived_draftungraded
Experimental context and source evidence
experimental_model
Purified pig renal Na,K-ATPase; 3.5 angstrom crystallography with rubidium.
limitations
Rubidium is a congener; a static purified structure is not a dietary depletion test.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Pig
plain_language
The pump has two sites that can trap a potassium-like ion during transport.
primary_references
[morth-2007-pump] Crystal structure of the sodium-potassium pump (2007). https://pubmed.ncbi.nlm.nih.gov/18075585/ DOI: 10.1038/nature06419
tissue_or_cell_type
Renal membrane enzyme
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 599–608
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified pig renal Na,K-ATPase; 3.5 angstrom crystallography with rubidium. · source_derived_draft · unverified_draft
### k-pump-two-occluded-sites The pig pump structure resolved two occluded rubidium ions at potassium transport sites in its alpha subunit. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The pump has two sites that can trap a potassium-like ion during transport. organism: Pig tissue_or_cell_type: Renal membrane enzyme experimental_model: Purified pig renal Na,K-ATPase; 3.5 angstrom crystallography with rubidium. limitations: Rubidium is a congener; a static purified structure is not a dietary depletion test. [morth-2007-pump] Crystal structure of the sodium-potassium pump (2007). https://pubmed.ncbi.nlm.nih.gov/18075585/ DOI: 10.1038/nature06419
Complete structured claim and evidence
Lowering bath K from 5.0 to 2.7 mM reduced ventricular pump current and increased intracellular sodium.
Extracellular potassium concentration → Sodium-potassium ATPase complexes source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Low extracellular potassium compromises sodium extrusion.
experimental_model
Rat ventricular patch clamp/Na fluorescence.
limitations
Acute bath manipulation; not dietary depletion.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rat
plain_language
With less extracellular potassium, sodium extrusion slowed.
primary_references
[aronsen-2015-cardiac] Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase alpha2 activity (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4376427/ DOI: 10.1113/jphysiol.2014.279893
tissue_or_cell_type
Ventricular myocytes
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 610–620
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat ventricular patch clamp/Na fluorescence. · source_derived_draft · unverified_draft
### k-low-cardiac-pump-current Lowering bath K from 5.0 to 2.7 mM reduced ventricular pump current and increased intracellular sodium. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: With less extracellular potassium, sodium extrusion slowed. organism: Rat tissue_or_cell_type: Ventricular myocytes experimental_model: Rat ventricular patch clamp/Na fluorescence. limitations: Acute bath manipulation; not dietary depletion. cross_nutrient: Low extracellular potassium compromises sodium extrusion. [aronsen-2015-cardiac] Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase alpha2 activity (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4376427/ DOI: 10.1113/jphysiol.2014.279893
Complete structured claim and evidence
Pump inhibition during low-K exposure increased sodium sensed by NCX and favored cellular calcium loading.
Sodium-potassium ATPase complexes → Na+/Ca2+ exchanger 1 / SLC8A1 source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium-to-sodium-to-calcium coupling is experimentally supported; dietary effect magnitude is untested.
experimental_model
Rat ventricular ion assays plus modeling.
limitations
NCX microdomain interpretation; source ouabain units differ between methods and figure legends.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rat
plain_language
Potassium-dependent sodium pumping helps the exchanger remove calcium.
primary_references
[aronsen-2015-cardiac] Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase alpha2 activity (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4376427/ DOI: 10.1113/jphysiol.2014.279893
tissue_or_cell_type
Ventricular myocytes
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 622–632
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat ventricular ion assays plus modeling. · source_derived_draft · unverified_draft
### k-low-cardiac-ncx-calcium Pump inhibition during low-K exposure increased sodium sensed by NCX and favored cellular calcium loading. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium-dependent sodium pumping helps the exchanger remove calcium. organism: Rat tissue_or_cell_type: Ventricular myocytes experimental_model: Rat ventricular ion assays plus modeling. limitations: NCX microdomain interpretation; source ouabain units differ between methods and figure legends. cross_nutrient: Potassium-to-sodium-to-calcium coupling is experimentally supported; dietary effect magnitude is untested. [aronsen-2015-cardiac] Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase alpha2 activity (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4376427/ DOI: 10.1113/jphysiol.2014.279893
Complete structured claim and evidence
Acute low-K superfusion hyperpolarized rat ventricular resting voltage despite increasing calcium transients.
Extracellular potassium concentration → Resting plasma-membrane potential source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
experimental_model
Rat ventricular voltage and calcium recordings.
limitations
Do not equate hyperpolarization with protection from arrhythmia.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rat
plain_language
A more negative resting voltage did not prevent calcium accumulation.
primary_references
[aronsen-2015-cardiac] Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase alpha2 activity (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4376427/ DOI: 10.1113/jphysiol.2014.279893
tissue_or_cell_type
Ventricle
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 634–643
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat ventricular voltage and calcium recordings. · source_derived_draft · unverified_draft
### k-low-cardiac-hyperpolarization Acute low-K superfusion hyperpolarized rat ventricular resting voltage despite increasing calcium transients. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A more negative resting voltage did not prevent calcium accumulation. organism: Rat tissue_or_cell_type: Ventricle experimental_model: Rat ventricular voltage and calcium recordings. limitations: Do not equate hyperpolarization with protection from arrhythmia. [aronsen-2015-cardiac] Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase alpha2 activity (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4376427/ DOI: 10.1113/jphysiol.2014.279893
Complete structured claim and evidence
Rabbit hearts exposed to 2.7 mM K showed increased CaMKII activity; KN-93 prevented low-K early afterdepolarizations and ventricular arrhythmia.
Extracellular potassium concentration → Ca2+/calmodulin-dependent protein kinase II family source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium depletion of the bath alters calcium-dependent signaling.
experimental_model
Isolated hearts; enzyme assay and inhibitor intervention.
limitations
Pharmacology is not genetic specificity; clinical efficacy was not tested.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rabbit and rat experimental series
plain_language
Calcium-sensitive kinase signaling contributed to electrical instability.
primary_references
[pezhouman-2015-camkii] Molecular Basis of Hypokalemia-Induced Ventricular Fibrillation (2015). https://pubmed.ncbi.nlm.nih.gov/26269574/ DOI: 10.1161/CIRCULATIONAHA.115.016217
tissue_or_cell_type
Ventricular myocardium
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 645–655
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated hearts; enzyme assay and inhibitor intervention. · source_derived_draft · unverified_draft
### k-low-activates-camkii Rabbit hearts exposed to 2.7 mM K showed increased CaMKII activity; KN-93 prevented low-K early afterdepolarizations and ventricular arrhythmia. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium-sensitive kinase signaling contributed to electrical instability. organism: Rabbit and rat experimental series tissue_or_cell_type: Ventricular myocardium experimental_model: Isolated hearts; enzyme assay and inhibitor intervention. limitations: Pharmacology is not genetic specificity; clinical efficacy was not tested. cross_nutrient: Potassium depletion of the bath alters calcium-dependent signaling. [pezhouman-2015-camkii] Molecular Basis of Hypokalemia-Induced Ventricular Fibrillation (2015). https://pubmed.ncbi.nlm.nih.gov/26269574/ DOI: 10.1161/CIRCULATIONAHA.115.016217
Complete structured claim and evidence
GS-967 suppressed hypokalemic early afterdepolarizations; simulations implicated CaMKII-enhanced late sodium current in a sodium/calcium feedback loop.
Cardiac late sodium current → Cardiac early afterdepolarizations source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Sodium entry and calcium loading interact during low extracellular potassium.
experimental_model
Low-K cardiac inhibition experiments and computational model.
limitations
The complete feedback sequence is model-supported, not every step directly measured.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rabbit/rat and mathematical model
plain_language
Persistent sodium entry helped sustain low-potassium electrical instability.
primary_references
[pezhouman-2015-camkii] Molecular Basis of Hypokalemia-Induced Ventricular Fibrillation (2015). https://pubmed.ncbi.nlm.nih.gov/26269574/ DOI: 10.1161/CIRCULATIONAHA.115.016217
tissue_or_cell_type
Ventricular myocardium
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 657–667
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Low-K cardiac inhibition experiments and computational model. · source_derived_draft · unverified_draft
### k-low-late-sodium-feedback GS-967 suppressed hypokalemic early afterdepolarizations; simulations implicated CaMKII-enhanced late sodium current in a sodium/calcium feedback loop. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Persistent sodium entry helped sustain low-potassium electrical instability. organism: Rabbit/rat and mathematical model tissue_or_cell_type: Ventricular myocardium experimental_model: Low-K cardiac inhibition experiments and computational model. limitations: The complete feedback sequence is model-supported, not every step directly measured. cross_nutrient: Sodium entry and calcium loading interact during low extracellular potassium. [pezhouman-2015-camkii] Molecular Basis of Hypokalemia-Induced Ventricular Fibrillation (2015). https://pubmed.ncbi.nlm.nih.gov/26269574/ DOI: 10.1161/CIRCULATIONAHA.115.016217
Complete structured claim and evidence
Low-K exposure increased calcium waves in ventricular and tubulated atrial cells, with a weaker response in untubulated atrial cells.
Extracellular potassium concentration → Propagating cardiac calcium waves source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
The calcium response to potassium depends on cellular transport organization.
experimental_model
Rat myocytes, 5.0 to 2.7 mM K, 3 minutes.
limitations
Architecture-dependent findings should not be generalized to all heart cells.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rat
plain_language
Internal membrane architecture changed how low potassium disturbed calcium.
primary_references
[tazmini-2020-cardiac] Hypokalemia Promotes Arrhythmia by Distinct Mechanisms in Atrial and Ventricular Myocytes (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7098435/ DOI: 10.1161/CIRCRESAHA.119.315641
tissue_or_cell_type
Atrial/ventricular myocardium
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 669–679
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat myocytes, 5.0 to 2.7 mM K, 3 minutes. · source_derived_draft · unverified_draft
### k-low-calcium-waves-tubules Low-K exposure increased calcium waves in ventricular and tubulated atrial cells, with a weaker response in untubulated atrial cells. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Internal membrane architecture changed how low potassium disturbed calcium. organism: Rat tissue_or_cell_type: Atrial/ventricular myocardium experimental_model: Rat myocytes, 5.0 to 2.7 mM K, 3 minutes. limitations: Architecture-dependent findings should not be generalized to all heart cells. cross_nutrient: The calcium response to potassium depends on cellular transport organization. [tazmini-2020-cardiac] Hypokalemia Promotes Arrhythmia by Distinct Mechanisms in Atrial and Ventricular Myocytes (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7098435/ DOI: 10.1161/CIRCRESAHA.119.315641
Complete structured claim and evidence
Untubulated atrial cells developed low-K early afterdepolarizations associated with sodium-current reactivation, hyperpolarization and brief action potentials.
Extracellular potassium concentration → Cardiac early afterdepolarizations source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Low extracellular potassium changes sodium-channel availability in this cell population.
experimental_model
Rat atrial electrophysiology and modeling.
limitations
Distinct from the calcium-overload route in tubulated cells.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rat
plain_language
Some atrial cells became unstable through sodium-channel behavior.
primary_references
[tazmini-2020-cardiac] Hypokalemia Promotes Arrhythmia by Distinct Mechanisms in Atrial and Ventricular Myocytes (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7098435/ DOI: 10.1161/CIRCRESAHA.119.315641
tissue_or_cell_type
Untubulated atrial myocytes
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 681–691
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat atrial electrophysiology and modeling. · source_derived_draft · unverified_draft
### k-low-atrial-sodium-reactivation Untubulated atrial cells developed low-K early afterdepolarizations associated with sodium-current reactivation, hyperpolarization and brief action potentials. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some atrial cells became unstable through sodium-channel behavior. organism: Rat tissue_or_cell_type: Untubulated atrial myocytes experimental_model: Rat atrial electrophysiology and modeling. limitations: Distinct from the calcium-overload route in tubulated cells. cross_nutrient: Low extracellular potassium changes sodium-channel availability in this cell population. [tazmini-2020-cardiac] Hypokalemia Promotes Arrhythmia by Distinct Mechanisms in Atrial and Ventricular Myocytes (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7098435/ DOI: 10.1161/CIRCRESAHA.119.315641
Complete structured claim and evidence
Low extracellular K accelerated hERG internalization and degradation; 0 versus 5 mM exposure strongly reduced mature surface channels.
Extracellular potassium concentration → Cell-surface hERG abundance source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
experimental_model
Transfected HEK293 cells, 6-12-hour low-K exposures.
limitations
Zero-K culture is more extreme than ordinary hypokalemia.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Human protein in HEK293 cells
plain_language
Potassium outside the cell helped retain a cardiac repolarizing channel.
primary_references
[guo-2009-herg] Extracellular K+ concentration controls cell surface density of IKr in rabbit hearts and of the HERG channel in human cell lines (2009). https://www.jci.org/articles/view/39027 DOI: 10.1172/JCI39027
tissue_or_cell_type
Heterologous culture
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 693–702
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected HEK293 cells, 6-12-hour low-K exposures. · source_derived_draft · unverified_draft
### k-low-herg-turnover Low extracellular K accelerated hERG internalization and degradation; 0 versus 5 mM exposure strongly reduced mature surface channels. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium outside the cell helped retain a cardiac repolarizing channel. organism: Human protein in HEK293 cells tissue_or_cell_type: Heterologous culture experimental_model: Transfected HEK293 cells, 6-12-hour low-K exposures. limitations: Zero-K culture is more extreme than ordinary hypokalemia. [guo-2009-herg] Extracellular K+ concentration controls cell surface density of IKr in rabbit hearts and of the HERG channel in human cell lines (2009). https://www.jci.org/articles/view/39027 DOI: 10.1172/JCI39027
Complete structured claim and evidence
Four weeks of 0.1% versus 0.62% dietary K produced hypokalemia, reduced ventricular IKr and prolonged corrected QT in rabbits.
Potassium → Cardiac rapidly activating delayed rectifier potassium current source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
experimental_model
Rabbit dietary experiment, four weeks.
limitations
Animal dietary finding does not establish human intake targets or a sole QT mechanism.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rabbit
plain_language
Sustained dietary restriction affected a cardiac recovery current.
primary_references
[guo-2009-herg] Extracellular K+ concentration controls cell surface density of IKr in rabbit hearts and of the HERG channel in human cell lines (2009). https://www.jci.org/articles/view/39027 DOI: 10.1172/JCI39027
tissue_or_cell_type
Ventricular myocardium
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 704–713
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rabbit dietary experiment, four weeks. · source_derived_draft · unverified_draft
### k-diet-rabbit-ikr Four weeks of 0.1% versus 0.62% dietary K produced hypokalemia, reduced ventricular IKr and prolonged corrected QT in rabbits. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sustained dietary restriction affected a cardiac recovery current. organism: Rabbit tissue_or_cell_type: Ventricular myocardium experimental_model: Rabbit dietary experiment, four weeks. limitations: Animal dietary finding does not establish human intake targets or a sole QT mechanism. [guo-2009-herg] Extracellular K+ concentration controls cell surface density of IKr in rabbit hearts and of the HERG channel in human cell lines (2009). https://www.jci.org/articles/view/39027 DOI: 10.1172/JCI39027
Complete structured claim and evidence
The combined 85 mM Na/9 mM K bath reduced M-wave area and tetanic force versus 147 mM Na/4 mM K.
Extracellular potassium concentration → Skeletal muscle excitability source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Reduced sodium and elevated potassium jointly impair excitability.
experimental_model
Isolated rat soleus, combined bath-ion perturbation.
limitations
Combined perturbation cannot be attributed to potassium alone; not dietary excess.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rat
plain_language
Both sodium and potassium gradients matter for muscle activation.
primary_references
[overgaard-1999-muscle] Relations between excitability and contractility in rat soleus muscle: role of the Na+-K+ pump and Na+/K+ gradients (1999). https://pubmed.ncbi.nlm.nih.gov/10373703/ DOI: 10.1111/j.1469-7793.1999.0215r.x
tissue_or_cell_type
Soleus muscle
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 715–725
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated rat soleus, combined bath-ion perturbation. · source_derived_draft · unverified_draft
### k-na-gradients-muscle-excitability The combined 85 mM Na/9 mM K bath reduced M-wave area and tetanic force versus 147 mM Na/4 mM K. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Both sodium and potassium gradients matter for muscle activation. organism: Rat tissue_or_cell_type: Soleus muscle experimental_model: Isolated rat soleus, combined bath-ion perturbation. limitations: Combined perturbation cannot be attributed to potassium alone; not dietary excess. cross_nutrient: Reduced sodium and elevated potassium jointly impair excitability. [overgaard-1999-muscle] Relations between excitability and contractility in rat soleus muscle: role of the Na+-K+ pump and Na+/K+ gradients (1999). https://pubmed.ncbi.nlm.nih.gov/10373703/ DOI: 10.1111/j.1469-7793.1999.0215r.x
Complete structured claim and evidence
Insulin stimulation of active Na-K transport restored M-wave area and force in the reduced-gradient soleus preparation.
Insulin → Skeletal muscle excitability source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Hormonal stimulation coordinates sodium extrusion and potassium entry.
experimental_model
Rat soleus in 85 mM Na/9 mM K.
limitations
Ex vivo rescue is not a clinical intervention recommendation.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rat
plain_language
Stimulating the shared sodium-potassium pump improved muscle responses.
primary_references
[overgaard-1999-muscle] Relations between excitability and contractility in rat soleus muscle: role of the Na+-K+ pump and Na+/K+ gradients (1999). https://pubmed.ncbi.nlm.nih.gov/10373703/ DOI: 10.1111/j.1469-7793.1999.0215r.x
tissue_or_cell_type
Soleus muscle
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 727–737
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat soleus in 85 mM Na/9 mM K. · source_derived_draft · unverified_draft
### k-insulin-muscle-pump-rescue Insulin stimulation of active Na-K transport restored M-wave area and force in the reduced-gradient soleus preparation. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Stimulating the shared sodium-potassium pump improved muscle responses. organism: Rat tissue_or_cell_type: Soleus muscle experimental_model: Rat soleus in 85 mM Na/9 mM K. limitations: Ex vivo rescue is not a clinical intervention recommendation. cross_nutrient: Hormonal stimulation coordinates sodium extrusion and potassium entry. [overgaard-1999-muscle] Relations between excitability and contractility in rat soleus muscle: role of the Na+-K+ pump and Na+/K+ gradients (1999). https://pubmed.ncbi.nlm.nih.gov/10373703/ DOI: 10.1111/j.1469-7793.1999.0215r.x
Complete structured claim and evidence
Rodent potassium depletion reversibly reduced muscle ouabain-binding sites and pump-mediated potassium uptake capacity.
Potassium → Sodium-potassium ATPase abundance source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium status alters machinery that also controls sodium transport.
experimental_model
Rat/mouse soleus and extensor digitorum longus; K-free diet, diuretic or K-binding-resin depletion models.
limitations
Diet, diuretic and resin models differ; abstract does not provide each regimen duration.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rat and mouse
plain_language
Depleted muscle had fewer functional sodium-potassium pumps.
primary_references
[norgaard-1981-muscle] Potassium depletion decreases the number of 3H-ouabain binding sites and the active Na-K transport in skeletal muscle (1981). https://www.nature.com/articles/293739a0 DOI: 10.1038/293739a0
tissue_or_cell_type
Soleus/extensor digitorum longus
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 739–749
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat/mouse soleus and extensor digitorum longus; K-free diet, diuretic or K-binding-resin depletion models. · source_derived_draft · unverified_draft
### k-depletion-muscle-pump-loss Rodent potassium depletion reversibly reduced muscle ouabain-binding sites and pump-mediated potassium uptake capacity. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Depleted muscle had fewer functional sodium-potassium pumps. organism: Rat and mouse tissue_or_cell_type: Soleus/extensor digitorum longus experimental_model: Rat/mouse soleus and extensor digitorum longus; K-free diet, diuretic or K-binding-resin depletion models. limitations: Diet, diuretic and resin models differ; abstract does not provide each regimen duration. cross_nutrient: Potassium status alters machinery that also controls sodium transport. [norgaard-1981-muscle] Potassium depletion decreases the number of 3H-ouabain binding sites and the active Na-K transport in skeletal muscle (1981). https://www.nature.com/articles/293739a0 DOI: 10.1038/293739a0
Complete structured claim and evidence
R528H mouse fibers displayed anomalous inward current at resting potentials, supporting a voltage-sensor leak mechanism.
CaV1.1 R528H variant → Voltage-sensor gating-pore current source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
experimental_model
Knock-in mouse fiber voltage clamp.
limitations
The leak is not equivalent to the normal calcium-conducting pore.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mouse
plain_language
An inherited calcium-channel variant added an abnormal leak.
primary_references
[wu-2012-hypopp] A calcium channel mutant mouse model of hypokalemic periodic paralysis (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3533564/ DOI: 10.1172/JCI66091
tissue_or_cell_type
Skeletal muscle
trigger_kind
machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 751–760
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Knock-in mouse fiber voltage clamp. · source_derived_draft · unverified_draft
### k-hypopp-gating-pore R528H mouse fibers displayed anomalous inward current at resting potentials, supporting a voltage-sensor leak mechanism. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inherited calcium-channel variant added an abnormal leak. organism: Mouse tissue_or_cell_type: Skeletal muscle experimental_model: Knock-in mouse fiber voltage clamp. limitations: The leak is not equivalent to the normal calcium-conducting pore. [wu-2012-hypopp] A calcium channel mutant mouse model of hypokalemic periodic paralysis (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3533564/ DOI: 10.1172/JCI66091
Complete structured claim and evidence
At 2 mM bath K, R528H muscle paradoxically depolarized and lost force while wild-type fibers hyperpolarized.
CaV1.1 R528H variant → Skeletal muscle excitability source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
A calcium-channel genetic defect changes potassium sensitivity of sodium-dependent muscle excitability.
experimental_model
4.75 to 2 mM K challenge; mouse muscle recordings.
limitations
Sex/genotype influenced susceptibility; no general dietary-paralysis claim.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mouse
plain_language
The same low-potassium exposure acted differently with inherited channel impairment.
primary_references
[wu-2012-hypopp] A calcium channel mutant mouse model of hypokalemic periodic paralysis (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3533564/ DOI: 10.1172/JCI66091
tissue_or_cell_type
Skeletal muscle
trigger_kind
machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 762–772
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 4.75 to 2 mM K challenge; mouse muscle recordings. · source_derived_draft · unverified_draft
### k-hypopp-low-k-depolarization At 2 mM bath K, R528H muscle paradoxically depolarized and lost force while wild-type fibers hyperpolarized. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same low-potassium exposure acted differently with inherited channel impairment. organism: Mouse tissue_or_cell_type: Skeletal muscle experimental_model: 4.75 to 2 mM K challenge; mouse muscle recordings. limitations: Sex/genotype influenced susceptibility; no general dietary-paralysis claim. cross_nutrient: A calcium-channel genetic defect changes potassium sensitivity of sodium-dependent muscle excitability. [wu-2012-hypopp] A calcium channel mutant mouse model of hypokalemic periodic paralysis (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3533564/ DOI: 10.1172/JCI66091
Complete structured claim and evidence
Glucose metabolism closed resting potassium channels in cell-attached rat beta-cell recordings.
D-glucose → Pancreatic beta-cell ATP-sensitive potassium current source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Carbohydrate metabolism regulates a potassium conductance rather than proving potassium supplementation benefit.
experimental_model
Cell-attached patch recordings in isolated rat pancreatic beta cells; glucose and metabolism perturbation.
limitations
The experiment does not establish dietary potassium control of insulin secretion.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rat
plain_language
The glucose fuel signal reduced potassium conductance.
primary_references
[ashcroft-1984-glucose] Glucose induces closure of single potassium channels in isolated rat pancreatic beta-cells (1984). https://www.nature.com/articles/312446a0 DOI: 10.1038/312446a0
tissue_or_cell_type
Pancreatic beta cells
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 774–784
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-attached patch recordings in isolated rat pancreatic beta cells; glucose and metabolism perturbation. · source_derived_draft · unverified_draft
### k-glucose-closes-beta-channel Glucose metabolism closed resting potassium channels in cell-attached rat beta-cell recordings. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The glucose fuel signal reduced potassium conductance. organism: Rat tissue_or_cell_type: Pancreatic beta cells experimental_model: Cell-attached patch recordings in isolated rat pancreatic beta cells; glucose and metabolism perturbation. limitations: The experiment does not establish dietary potassium control of insulin secretion. cross_nutrient: Carbohydrate metabolism regulates a potassium conductance rather than proving potassium supplementation benefit. [ashcroft-1984-glucose] Glucose induces closure of single potassium channels in isolated rat pancreatic beta-cells (1984). https://www.nature.com/articles/312446a0 DOI: 10.1038/312446a0
Complete structured claim and evidence
Free ATP and nonhydrolyzable ATP analogues inhibited beta-cell KATP channels without requiring phosphorylation.
ATP → Pancreatic beta-cell ATP-sensitive potassium current source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Free ATP must be distinguished from its magnesium complex.
experimental_model
Rat beta-cell inside-out patches.
limitations
Excised patches do not reproduce all intact-cell metabolic regulation.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rat
plain_language
ATP can close the potassium channel through nucleotide regulation.
primary_references
[ashcroft-1989-magnesium] ATP-sensitive K+ channels in rat pancreatic beta-cells: modulation by ATP and Mg2+ ions (1989). https://pmc.ncbi.nlm.nih.gov/articles/PMC1189219/ DOI: 10.1113/jphysiol.1989.sp017765
tissue_or_cell_type
Pancreatic beta-cell membrane
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 786–796
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat beta-cell inside-out patches. · source_derived_draft · unverified_draft
### k-beta-atp-inhibition Free ATP and nonhydrolyzable ATP analogues inhibited beta-cell KATP channels without requiring phosphorylation. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: ATP can close the potassium channel through nucleotide regulation. organism: Rat tissue_or_cell_type: Pancreatic beta-cell membrane experimental_model: Rat beta-cell inside-out patches. limitations: Excised patches do not reproduce all intact-cell metabolic regulation. cross_nutrient: Free ATP must be distinguished from its magnesium complex. [ashcroft-1989-magnesium] ATP-sensitive K+ channels in rat pancreatic beta-cells: modulation by ATP and Mg2+ ions (1989). https://pmc.ncbi.nlm.nih.gov/articles/PMC1189219/ DOI: 10.1113/jphysiol.1989.sp017765
Complete structured claim and evidence
Adding 2 mM Mg shifted apparent total-ATP inhibition from Ki 4 to 26 micromolar in excised beta-cell patches.
Mg2+ → Pancreatic beta-cell ATP-sensitive potassium current source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Magnesium-nucleotide chemistry modifies potassium-channel gating; no dietary magnesium effect quantified.
experimental_model
Inside-out rat patches; Mg-free versus 2 mM Mg.
limitations
Assay concentrations are not clinical magnesium thresholds.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rat
plain_language
Magnesium changed how the potassium channel responded to total ATP.
primary_references
[ashcroft-1989-magnesium] ATP-sensitive K+ channels in rat pancreatic beta-cells: modulation by ATP and Mg2+ ions (1989). https://pmc.ncbi.nlm.nih.gov/articles/PMC1189219/ DOI: 10.1113/jphysiol.1989.sp017765
tissue_or_cell_type
Pancreatic beta-cell membrane
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 798–808
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inside-out rat patches; Mg-free versus 2 mM Mg. · source_derived_draft · unverified_draft
### k-beta-mg-atp-speciation Adding 2 mM Mg shifted apparent total-ATP inhibition from Ki 4 to 26 micromolar in excised beta-cell patches. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Magnesium changed how the potassium channel responded to total ATP. organism: Rat tissue_or_cell_type: Pancreatic beta-cell membrane experimental_model: Inside-out rat patches; Mg-free versus 2 mM Mg. limitations: Assay concentrations are not clinical magnesium thresholds. cross_nutrient: Magnesium-nucleotide chemistry modifies potassium-channel gating; no dietary magnesium effect quantified. [ashcroft-1989-magnesium] ATP-sensitive K+ channels in rat pancreatic beta-cells: modulation by ATP and Mg2+ ions (1989). https://pmc.ncbi.nlm.nih.gov/articles/PMC1189219/ DOI: 10.1113/jphysiol.1989.sp017765
Complete structured claim and evidence
MgADP potentiated cloned Kir6.2/SUR1 current through intact SUR1 nucleotide-binding machinery.
Magnesium-ADP complex → Kir6.2-SUR1 ATP-sensitive potassium channel source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
MgADP supplies a magnesium-dependent regulatory input to potassium conductance.
experimental_model
Xenopus oocyte cloned-channel patches.
limitations
Heterologous channel biochemistry, not nutritional magnesium depletion.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Xenopus expression system
plain_language
Magnesium-bound ADP helps keep this potassium channel active.
primary_references
[gribble-1997-sur1] The essential role of the Walker A motifs of SUR1 in K-ATP channel activation by Mg-ADP and diazoxide (1997). https://pmc.ncbi.nlm.nih.gov/articles/PMC1169713/ DOI: 10.1093/emboj/16.6.1145
tissue_or_cell_type
Oocyte membrane
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 810–820
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Xenopus oocyte cloned-channel patches. · source_derived_draft · unverified_draft
### k-mgadp-sur1-activation MgADP potentiated cloned Kir6.2/SUR1 current through intact SUR1 nucleotide-binding machinery. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Magnesium-bound ADP helps keep this potassium channel active. organism: Xenopus expression system tissue_or_cell_type: Oocyte membrane experimental_model: Xenopus oocyte cloned-channel patches. limitations: Heterologous channel biochemistry, not nutritional magnesium depletion. cross_nutrient: MgADP supplies a magnesium-dependent regulatory input to potassium conductance. [gribble-1997-sur1] The essential role of the Walker A motifs of SUR1 in K-ATP channel activation by Mg-ADP and diazoxide (1997). https://pmc.ncbi.nlm.nih.gov/articles/PMC1169713/ DOI: 10.1093/emboj/16.6.1145
Complete structured claim and evidence
SUR1 K719A or K1384M substitution impaired MgADP potentiation of cloned KATP currents.
SUR1 K719A variant → Kir6.2-SUR1 ATP-sensitive potassium channel source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
A machinery defect interrupts magnesium-nucleotide regulation without demonstrating ion deficiency.
experimental_model
Mutant versus wild-type Xenopus patches.
limitations
Engineered substitutions are not evidence of dietary K or Mg deficiency.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Xenopus expression system
plain_language
Damaged nucleotide machinery can disrupt potassium-channel regulation.
primary_references
[gribble-1997-sur1] The essential role of the Walker A motifs of SUR1 in K-ATP channel activation by Mg-ADP and diazoxide (1997). https://pmc.ncbi.nlm.nih.gov/articles/PMC1169713/ DOI: 10.1093/emboj/16.6.1145
tissue_or_cell_type
Oocyte membrane
trigger_kind
machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 822–832
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mutant versus wild-type Xenopus patches. · source_derived_draft · unverified_draft
### k-sur1-mutations-mgadp SUR1 K719A or K1384M substitution impaired MgADP potentiation of cloned KATP currents. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Damaged nucleotide machinery can disrupt potassium-channel regulation. organism: Xenopus expression system tissue_or_cell_type: Oocyte membrane experimental_model: Mutant versus wild-type Xenopus patches. limitations: Engineered substitutions are not evidence of dietary K or Mg deficiency. cross_nutrient: A machinery defect interrupts magnesium-nucleotide regulation without demonstrating ion deficiency. [gribble-1997-sur1] The essential role of the Walker A motifs of SUR1 in K-ATP channel activation by Mg-ADP and diazoxide (1997). https://pmc.ncbi.nlm.nih.gov/articles/PMC1169713/ DOI: 10.1093/emboj/16.6.1145
Complete structured claim and evidence
Experimental depletion lowered clamp insulin response by 26% and glucose disposal by 27.4%; estimated tissue insulin sensitivity was unchanged.
Potassium → Insulin secretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium depletion altered carbohydrate handling; the precise cellular link remains unmeasured.
experimental_contrast
{"combination": "single", "comparator": "Before depletion in the reported clamp study", "conditions": [{"entity_slug": "potassium", "state": "Experimentally depleted"}], "effect_direction": "decrease", "endpoint": "Clamp insulin response", "intervention": "Experimental potassium depletion"} Comparison extracted from the existing source-pinned Rowe 1980 claim (PMID 6991855); no new primary full-text access in this pass. The raw supports/positive relationship is retained independently.
experimental_model
Seven healthy young men; 7-8 days, 40 mEq K/day diet plus 60 g/day sodium polystyrene sulfonate; 2-hour hyperglycemic clamp 125 mg/dL above baseline.
limitations
Seven men; diet-plus-resin exposure. No direct beta-cell channel measurement.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Human
plain_language
Depletion impaired glucose handling alongside a smaller insulin response.
primary_references
[rowe-1980-depletion] Effect of experimental potassium deficiency on glucose and insulin metabolism (1980). https://www.sciencedirect.com/science/article/pii/0026049580900748 DOI: 10.1016/0026-0495(80)90074-8
tissue_or_cell_type
Systemic glucose/insulin response
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 834–844
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Seven healthy young men; 7-8 days, 40 mEq K/day diet plus 60 g/day sodium polystyrene sulfonate; 2-hour hyperglycemic clamp 125 mg/dL above baseline. · source_derived_draft · unverified_draft
### k-human-depletion-insulin Experimental depletion lowered clamp insulin response by 26% and glucose disposal by 27.4%; estimated tissue insulin sensitivity was unchanged. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Depletion impaired glucose handling alongside a smaller insulin response. organism: Human tissue_or_cell_type: Systemic glucose/insulin response experimental_model: Seven healthy young men; 7-8 days, 40 mEq K/day diet plus 60 g/day sodium polystyrene sulfonate; 2-hour hyperglycemic clamp 125 mg/dL above baseline. limitations: Seven men; diet-plus-resin exposure. No direct beta-cell channel measurement. cross_nutrient: Potassium depletion altered carbohydrate handling; the precise cellular link remains unmeasured. [rowe-1980-depletion] Effect of experimental potassium deficiency on glucose and insulin metabolism (1980). https://www.sciencedirect.com/science/article/pii/0026049580900748 DOI: 10.1016/0026-0495(80)90074-8
Complete structured claim and evidence
Five depleted subjects had impaired oral glucose tolerance; two tested intravenously did not, and insulin-resistance tests were negative.
Potassium → Glucose tolerance source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
experimental_model
Seven experimentally depleted subjects, mean deficit 326 mEq; five oral and two intravenous glucose tests, followed by repletion.
limitations
Different small subject groups, not randomized route comparison. No contradiction with a scoped clamp result.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Human
plain_language
The measured glucose effect depended on the test and was mild.
primary_references
[gorden-1973-depletion] Glucose Intolerance with Hypokalemia: Failure of Short-term Potassium Depletion in Normal Subjects to Reproduce the Glucose and Insulin Abnormalities of Clinical Hypokalemia (1973). https://diabetesjournals.org/diabetes/article-pdf/22/7/544/347377/22-7-544.pdf DOI: 10.2337/diab.22.7.544
tissue_or_cell_type
Systemic glucose regulation
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 846–855
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Seven experimentally depleted subjects, mean deficit 326 mEq; five oral and two intravenous glucose tests, followed by repletion. · source_derived_draft · unverified_draft
### k-human-depletion-route-boundary Five depleted subjects had impaired oral glucose tolerance; two tested intravenously did not, and insulin-resistance tests were negative. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The measured glucose effect depended on the test and was mild. organism: Human tissue_or_cell_type: Systemic glucose regulation experimental_model: Seven experimentally depleted subjects, mean deficit 326 mEq; five oral and two intravenous glucose tests, followed by repletion. limitations: Different small subject groups, not randomized route comparison. No contradiction with a scoped clamp result. [gorden-1973-depletion] Glucose Intolerance with Hypokalemia: Failure of Short-term Potassium Depletion in Normal Subjects to Reproduce the Glucose and Insulin Abnormalities of Clinical Hypokalemia (1973). https://diabetesjournals.org/diabetes/article-pdf/22/7/544/347377/22-7-544.pdf DOI: 10.2337/diab.22.7.544
Complete structured claim and evidence
K-free medium triggered NLRP3-dependent IL-1beta release in primed macrophages, accompanying intracellular K loss.
Intracellular potassium concentration → NLRP3 inflammasome source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
experimental_model
LPS-primed mouse macrophages, 0 versus 5 mM K; response by 30 minutes.
limitations
Artificial cellular depletion; not a blood threshold or dietary inflammation experiment.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mouse
plain_language
Experimentally losing cellular potassium could trigger this immune sensor.
primary_references
[munoz-2013-nlrp3] K+ efflux is the Common Trigger of NLRP3 inflammasome Activation by Bacterial Toxins and Particulate Matter (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3730833/ DOI: 10.1016/j.immuni.2013.05.016
tissue_or_cell_type
Bone-marrow macrophages
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 857–866
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · LPS-primed mouse macrophages, 0 versus 5 mM K; response by 30 minutes. · source_derived_draft · unverified_draft
### k-macrophage-loss-nlrp3 K-free medium triggered NLRP3-dependent IL-1beta release in primed macrophages, accompanying intracellular K loss. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Experimentally losing cellular potassium could trigger this immune sensor. organism: Mouse tissue_or_cell_type: Bone-marrow macrophages experimental_model: LPS-primed mouse macrophages, 0 versus 5 mM K; response by 30 minutes. limitations: Artificial cellular depletion; not a blood threshold or dietary inflammation experiment. [munoz-2013-nlrp3] K+ efflux is the Common Trigger of NLRP3 inflammasome Activation by Bacterial Toxins and Particulate Matter (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3730833/ DOI: 10.1016/j.immuni.2013.05.016
Complete structured claim and evidence
Raising extracellular K to 45 mM maximally inhibited NLRP3 responses to the tested toxins and particles.
Extracellular potassium concentration → NLRP3 inflammasome source_derived_draftungraded
Experimental context and source evidence
experimental_model
Primed mouse macrophages, extracellular-K titration.
exposure
Artificial extracellular potassium elevation; not dietary excess.
limitations
Stimulus-specific; does not justify elevating blood potassium.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mouse
plain_language
Reducing the outward potassium gradient blocked these activation routes.
primary_references
[munoz-2013-nlrp3] K+ efflux is the Common Trigger of NLRP3 inflammasome Activation by Bacterial Toxins and Particulate Matter (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3730833/ DOI: 10.1016/j.immuni.2013.05.016
tissue_or_cell_type
Bone-marrow macrophages
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 868–878
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primed mouse macrophages, extracellular-K titration. · source_derived_draft · unverified_draft
### k-high-medium-nlrp3-block Raising extracellular K to 45 mM maximally inhibited NLRP3 responses to the tested toxins and particles. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reducing the outward potassium gradient blocked these activation routes. organism: Mouse tissue_or_cell_type: Bone-marrow macrophages experimental_model: Primed mouse macrophages, extracellular-K titration. limitations: Stimulus-specific; does not justify elevating blood potassium. exposure: Artificial extracellular potassium elevation; not dietary excess. [munoz-2013-nlrp3] K+ efflux is the Common Trigger of NLRP3 inflammasome Activation by Bacterial Toxins and Particulate Matter (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3730833/ DOI: 10.1016/j.immuni.2013.05.016
Complete structured claim and evidence
NEK7 loss blocked inflammasome assembly downstream of preserved K efflux; 50 mM KCl prevented the induced NEK7-NLRP3 interaction.
NIMA-related kinase 7 / NEK7 → NLRP3 inflammasome source_derived_draftungraded
Experimental context and source evidence
experimental_model
Mouse macrophages with Nek7 deletion/reconstitution; ATP, nigericin or gramicidin; high-K control, interaction assays.
limitations
NEK7 catalytic activity was dispensable; this is not proof of potassium binding directly to NEK7.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mouse
plain_language
Potassium loss signals through an assembly protein before caspase activation.
primary_references
[he-2016-nek7] NEK7 is an essential mediator of NLRP3 activation downstream of potassium efflux (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4810788/ DOI: 10.1038/nature16959
tissue_or_cell_type
Bone-marrow macrophages
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 880–889
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse macrophages with Nek7 deletion/reconstitution; ATP, nigericin or gramicidin; high-K control, interaction assays. · source_derived_draft · unverified_draft
### k-efflux-nek7-assembly NEK7 loss blocked inflammasome assembly downstream of preserved K efflux; 50 mM KCl prevented the induced NEK7-NLRP3 interaction. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium loss signals through an assembly protein before caspase activation. organism: Mouse tissue_or_cell_type: Bone-marrow macrophages experimental_model: Mouse macrophages with Nek7 deletion/reconstitution; ATP, nigericin or gramicidin; high-K control, interaction assays. limitations: NEK7 catalytic activity was dispensable; this is not proof of potassium binding directly to NEK7. [he-2016-nek7] NEK7 is an essential mediator of NLRP3 activation downstream of potassium efflux (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4810788/ DOI: 10.1038/nature16959
Complete structured claim and evidence
Imiquimod and CL097 activated NLRP3 without requiring potassium efflux in the studied myeloid-cell experiments.
Imiquimod → NLRP3 inflammasome source_derived_draftungraded
Experimental context and source evidence
experimental_model
Myeloid-cell inflammasome experiments using imiquimod and CL097, potassium-efflux tests and mitochondrial target analysis.
limitations
Stimulus-specific boundary, not opposing evidence for the toxin/particle experiments.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mouse experimental systems
plain_language
Some drug-triggered inflammasome routes bypass potassium loss.
primary_references
[gross-2016-independent] K+ Efflux-Independent NLRP3 Inflammasome Activation by Small Molecules Targeting Mitochondria (2016). https://pubmed.ncbi.nlm.nih.gov/27692612/ DOI: 10.1016/j.immuni.2016.08.010
tissue_or_cell_type
Myeloid cells
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 891–900
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Myeloid-cell inflammasome experiments using imiquimod and CL097, potassium-efflux tests and mitochondrial target analysis. · source_derived_draft · unverified_draft
### k-independent-drug-nlrp3 Imiquimod and CL097 activated NLRP3 without requiring potassium efflux in the studied myeloid-cell experiments. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some drug-triggered inflammasome routes bypass potassium loss. organism: Mouse experimental systems tissue_or_cell_type: Myeloid cells experimental_model: Myeloid-cell inflammasome experiments using imiquimod and CL097, potassium-efflux tests and mitochondrial target analysis. limitations: Stimulus-specific boundary, not opposing evidence for the toxin/particle experiments. [gross-2016-independent] K+ Efflux-Independent NLRP3 Inflammasome Activation by Small Molecules Targeting Mitochondria (2016). https://pubmed.ncbi.nlm.nih.gov/27692612/ DOI: 10.1016/j.immuni.2016.08.010
Complete structured claim and evidence
Elevated intracellular K suppressed TCR-driven AKT-mTOR signaling through a PP2A-dependent process.
Intracellular potassium concentration → T-cell AKT-mTOR signaling source_derived_draftungraded
Experimental context and source evidence
experimental_model
High-K mouse/human T-cell cultures; PP2A perturbations.
limitations
PP2A dependence does not demonstrate direct K binding; no diet manipulation.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mouse and human
plain_language
Local potassium accumulation dampened T-cell activation signals.
primary_references
[eil-2016-tcells] Ionic immune suppression within the tumour microenvironment limits T cell effector function (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5204372/ DOI: 10.1038/nature19364
tissue_or_cell_type
T cells
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 902–911
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-K mouse/human T-cell cultures; PP2A perturbations. · source_derived_draft · unverified_draft
### k-tcell-pp2a-suppression Elevated intracellular K suppressed TCR-driven AKT-mTOR signaling through a PP2A-dependent process. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Local potassium accumulation dampened T-cell activation signals. organism: Mouse and human tissue_or_cell_type: T cells experimental_model: High-K mouse/human T-cell cultures; PP2A perturbations. limitations: PP2A dependence does not demonstrate direct K binding; no diet manipulation. [eil-2016-tcells] Ionic immune suppression within the tumour microenvironment limits T cell effector function (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5204372/ DOI: 10.1038/nature19364
Complete structured claim and evidence
Kv1.3 overexpression lowered intracellular K and improved antitumor T-cell function; engineered cells improved melanoma control in mice.
Kv1.3 / KCNA3 → T-cell effector function source_derived_draftungraded
Experimental context and source evidence
experimental_model
Engineered T cells, culture and adoptive transfer.
limitations
Genetic cell intervention cannot be translated into a dietary potassium claim.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mouse with human-cell complementary assays
plain_language
Increasing potassium exit rescued cells in this tumor model.
primary_references
[eil-2016-tcells] Ionic immune suppression within the tumour microenvironment limits T cell effector function (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5204372/ DOI: 10.1038/nature19364
tissue_or_cell_type
Tumor-infiltrating T cells
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 913–922
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Engineered T cells, culture and adoptive transfer. · source_derived_draft · unverified_draft
### k-tcell-kv13-efflux Kv1.3 overexpression lowered intracellular K and improved antitumor T-cell function; engineered cells improved melanoma control in mice. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Increasing potassium exit rescued cells in this tumor model. organism: Mouse with human-cell complementary assays tissue_or_cell_type: Tumor-infiltrating T cells experimental_model: Engineered T cells, culture and adoptive transfer. limitations: Genetic cell intervention cannot be translated into a dietary potassium claim. [eil-2016-tcells] Ionic immune suppression within the tumour microenvironment limits T cell effector function (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5204372/ DOI: 10.1038/nature19364
Complete structured claim and evidence
The 12-week KCl pilot found no significant between-group improvement in primary glucose AUC or OGTT insulin measures.
Potassium chloride → Glucose tolerance source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
experimental_model
Prediabetes pilot, 40 mEq/day KCl, 27 completers.
limitations
Underpowered pilot; absence of significance is not proof of no effect.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Human
plain_language
The trial did not establish better glucose tolerance.
primary_references
[chatterjee-2017-pilot] Effects of potassium supplements on glucose metabolism in African Americans with prediabetes: a pilot trial (2017). https://pmc.ncbi.nlm.nih.gov/articles/PMC5698842/ DOI: 10.3945/ajcn.117.161570
tissue_or_cell_type
Systemic glucose regulation
trigger_kind
biomarker_context Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 924–933
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prediabetes pilot, 40 mEq/day KCl, 27 completers. · source_derived_draft · unverified_draft
### k-pilot-ogtt-null The 12-week KCl pilot found no significant between-group improvement in primary glucose AUC or OGTT insulin measures. Condition category: biomarker_context nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The trial did not establish better glucose tolerance. organism: Human tissue_or_cell_type: Systemic glucose regulation experimental_model: Prediabetes pilot, 40 mEq/day KCl, 27 completers. limitations: Underpowered pilot; absence of significance is not proof of no effect. [chatterjee-2017-pilot] Effects of potassium supplements on glucose metabolism in African Americans with prediabetes: a pilot trial (2017). https://pmc.ncbi.nlm.nih.gov/articles/PMC5698842/ DOI: 10.3945/ajcn.117.161570
Complete structured claim and evidence
Fasting glucose changed -1.1 versus +6.1 mg/dL with KCl versus placebo, a secondary endpoint difference (P=0.03).
Potassium chloride → Fasting plasma glucose source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
experimental_model
Same 12-week prediabetes pilot.
limitations
Small sample and multiple endpoints; no diabetes-prevention endpoint.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Human
plain_language
Fasting glucose worsened less in the supplemented group.
primary_references
[chatterjee-2017-pilot] Effects of potassium supplements on glucose metabolism in African Americans with prediabetes: a pilot trial (2017). https://pmc.ncbi.nlm.nih.gov/articles/PMC5698842/ DOI: 10.3945/ajcn.117.161570
tissue_or_cell_type
Blood
trigger_kind
biomarker_context Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 935–944
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Same 12-week prediabetes pilot. · source_derived_draft · unverified_draft
### k-pilot-fasting-glucose Fasting glucose changed -1.1 versus +6.1 mg/dL with KCl versus placebo, a secondary endpoint difference (P=0.03). Condition category: biomarker_context nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Fasting glucose worsened less in the supplemented group. organism: Human tissue_or_cell_type: Blood experimental_model: Same 12-week prediabetes pilot. limitations: Small sample and multiple endpoints; no diabetes-prevention endpoint. [chatterjee-2017-pilot] Effects of potassium supplements on glucose metabolism in African Americans with prediabetes: a pilot trial (2017). https://pmc.ncbi.nlm.nih.gov/articles/PMC5698842/ DOI: 10.3945/ajcn.117.161570
Complete structured claim and evidence
Both potassium salts improved beta-cell-function estimates; only citrate improved insulin-sensitivity estimates in this small normokalemic pilot.
Potassium citrate → HOMA-IR estimate of insulin resistance source_derived_draftungraded
Experimental context and source evidence
availability_state
biomarker_context Imported condition classification; unverified.
cross_nutrient
Potassium and accompanying alkali cannot be treated as an identical intervention.
experimental_model
Eleven non-acidotic normokalemic adults, 7 men/4 women, ages 47-63; double-blind placebo-controlled KCl/K-citrate 90 mEq/day, two weeks each.
limitations
Eleven subjects, short duration and surrogate estimates; no established molecular pathway or prevention effect.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Human
plain_language
The accompanying anion changed the observed metabolic response.
primary_references
[conen-2016-pilot] Effects of potassium citrate or potassium chloride in patients with combined glucose intolerance: A placebo-controlled pilot study (2016). https://www.sciencedirect.com/science/article/abs/pii/S105687271630054X DOI: 10.1016/j.jdiacomp.2016.03.017
tissue_or_cell_type
Systemic glucose regulation
trigger_kind
biomarker_context Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 946–956
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Eleven non-acidotic normokalemic adults, 7 men/4 women, ages 47-63; double-blind placebo-controlled KCl/K-citrate 90 mEq/day, two weeks each. · source_derived_draft · unverified_draft
### k-salt-glycemic-anion-boundary Both potassium salts improved beta-cell-function estimates; only citrate improved insulin-sensitivity estimates in this small normokalemic pilot. Condition category: biomarker_context nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The accompanying anion changed the observed metabolic response. organism: Human tissue_or_cell_type: Systemic glucose regulation experimental_model: Eleven non-acidotic normokalemic adults, 7 men/4 women, ages 47-63; double-blind placebo-controlled KCl/K-citrate 90 mEq/day, two weeks each. limitations: Eleven subjects, short duration and surrogate estimates; no established molecular pathway or prevention effect. cross_nutrient: Potassium and accompanying alkali cannot be treated as an identical intervention. [conen-2016-pilot] Effects of potassium citrate or potassium chloride in patients with combined glucose intolerance: A placebo-controlled pilot study (2016). https://www.sciencedirect.com/science/article/abs/pii/S105687271630054X DOI: 10.1016/j.jdiacomp.2016.03.017
Complete structured claim and evidence
Potassium-deficient feeding increased urinary ammonium excretion before detectable hypokalemia in the studied rats.
Potassium → Urinary ammonium excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy.
endpoint
Potassium-deficient feeding increased urinary ammonium excretion before detectable hypokalemia in the studied rats.
experimental-exposure
Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.
experimental_model
Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.
limitations
Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
The kidney changed nitrogen and acid excretion before blood potassium fell.
primary_references
[hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011
tissue_or_cell_type
renal proximal tubule and whole-kidney excretion
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 958–970
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. · source_derived_draft · unverified_draft
### k-deprivation-early-ammonium Potassium-deficient feeding increased urinary ammonium excretion before detectable hypokalemia in the studied rats. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney changed nitrogen and acid excretion before blood potassium fell. organism: Rattus norvegicus tissue_or_cell_type: renal proximal tubule and whole-kidney excretion experimental_model: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. limitations: Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation. cross_nutrient: Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy. experimental-exposure: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. endpoint: Potassium-deficient feeding increased urinary ammonium excretion before detectable hypokalemia in the studied rats. [hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011
Complete structured claim and evidence
Potassium deprivation increased renal SNAT3/SN1 expression in the rat time course.
Potassium → SNAT3 / SLC38A3 source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy.
endpoint
Potassium deprivation increased renal SNAT3/SN1 expression in the rat time course.
experimental-exposure
Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.
experimental_model
Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.
limitations
Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
More glutamine transporter was detected in the kidney, supporting substrate delivery to the ammonia pathway.
primary_references
[hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011
tissue_or_cell_type
renal proximal tubule and whole-kidney excretion
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 972–984
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. · source_derived_draft · unverified_draft
### k-deprivation-snat3 Potassium deprivation increased renal SNAT3/SN1 expression in the rat time course. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: More glutamine transporter was detected in the kidney, supporting substrate delivery to the ammonia pathway. organism: Rattus norvegicus tissue_or_cell_type: renal proximal tubule and whole-kidney excretion experimental_model: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. limitations: Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation. cross_nutrient: Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy. experimental-exposure: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. endpoint: Potassium deprivation increased renal SNAT3/SN1 expression in the rat time course. [hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011
Complete structured claim and evidence
Potassium deprivation increased renal phosphate-dependent glutaminase expression in the studied rats.
Potassium → Kidney-type glutaminase / GLS source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy.
endpoint
Potassium deprivation increased renal phosphate-dependent glutaminase expression in the studied rats.
experimental-exposure
Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.
experimental_model
Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.
limitations
Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
The first glutamine-deaminating enzyme increased; glutamate and ammonium are separate products in this pathway.
primary_references
[hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011
tissue_or_cell_type
renal proximal tubule and whole-kidney excretion
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 986–998
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. · source_derived_draft · unverified_draft
### k-deprivation-gls Potassium deprivation increased renal phosphate-dependent glutaminase expression in the studied rats. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The first glutamine-deaminating enzyme increased; glutamate and ammonium are separate products in this pathway. organism: Rattus norvegicus tissue_or_cell_type: renal proximal tubule and whole-kidney excretion experimental_model: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. limitations: Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation. cross_nutrient: Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy. experimental-exposure: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. endpoint: Potassium deprivation increased renal phosphate-dependent glutaminase expression in the studied rats. [hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011
Complete structured claim and evidence
Potassium deprivation increased renal glutamate dehydrogenase expression in the studied rats.
Potassium → GLUD1 source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy.
endpoint
Potassium deprivation increased renal glutamate dehydrogenase expression in the studied rats.
experimental-exposure
Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.
experimental_model
Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.
limitations
Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
A second ammonia-producing enzyme increased; this connects glutamate nitrogen to ammonium and its carbon skeleton to 2-oxoglutarate.
primary_references
[hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011
tissue_or_cell_type
renal proximal tubule and whole-kidney excretion
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1000–1012
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. · source_derived_draft · unverified_draft
### k-deprivation-glud1 Potassium deprivation increased renal glutamate dehydrogenase expression in the studied rats. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second ammonia-producing enzyme increased; this connects glutamate nitrogen to ammonium and its carbon skeleton to 2-oxoglutarate. organism: Rattus norvegicus tissue_or_cell_type: renal proximal tubule and whole-kidney excretion experimental_model: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. limitations: Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation. cross_nutrient: Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy. experimental-exposure: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. endpoint: Potassium deprivation increased renal glutamate dehydrogenase expression in the studied rats. [hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011
Complete structured claim and evidence
Potassium deprivation increased renal phosphoenolpyruvate carboxykinase expression in the studied rats.
Potassium → Cytosolic phosphoenolpyruvate carboxykinase / PCK1 source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy.
endpoint
Potassium deprivation increased renal phosphoenolpyruvate carboxykinase expression in the studied rats.
experimental-exposure
Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.
experimental_model
Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.
limitations
Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
The carbon-processing arm of the ammoniagenic/gluconeogenic pathway adapted alongside the nitrogen-releasing enzymes.
primary_references
[hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011
tissue_or_cell_type
renal proximal tubule and whole-kidney excretion
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1014–1026
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. · source_derived_draft · unverified_draft
### k-deprivation-pck1 Potassium deprivation increased renal phosphoenolpyruvate carboxykinase expression in the studied rats. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The carbon-processing arm of the ammoniagenic/gluconeogenic pathway adapted alongside the nitrogen-releasing enzymes. organism: Rattus norvegicus tissue_or_cell_type: renal proximal tubule and whole-kidney excretion experimental_model: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. limitations: Dietary deprivation precedes detectable hypokalemia here; protein expression does not independently establish transport flux or quantify net bicarbonate generation. cross_nutrient: Potassium deprivation changes glutamine nitrogen metabolism and sodium-coupled glutamine transport; these experiments did not manipulate dietary protein adequacy. experimental-exposure: Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments. endpoint: Potassium deprivation increased renal phosphoenolpyruvate carboxykinase expression in the studied rats. [hossain-2011-k-ammoniagenesis] Cellular and molecular basis of increased ammoniagenesis in potassium deprivation (2011). https://journals.physiology.org/doi/full/10.1152/ajprenal.00010.2011 DOI: 10.1152/ajprenal.00010.2011
Complete structured claim and evidence
Diet-induced hypokalemia decreased glutamine synthetase expression throughout the mouse proximal tubule.
Potassium → Glutamine synthetase / GLUL source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
endpoint
Diet-induced hypokalemia decreased glutamine synthetase expression throughout the mouse proximal tubule.
experimental-exposure
Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays.
experimental_model
Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays.
limitations
Expression and localization were measured; the quantitative contribution of GLUL to total flux was not isolated.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
Less ammonia-recycling enzyme was present in this compartment, potentially leaving more ammonia available for excretion.
primary_references
[verlander-2013-gs] Expression of glutamine synthetase in the mouse kidney: localization in multiple epithelial cell types and differential regulation by hypokalemia (2013). https://pubmed.ncbi.nlm.nih.gov/23804452/ DOI: 10.1152/ajprenal.00030.2013
tissue_or_cell_type
renal proximal tubule
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1028–1039
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays. · source_derived_draft · unverified_draft
### k-depletion-proximal-glul Diet-induced hypokalemia decreased glutamine synthetase expression throughout the mouse proximal tubule. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less ammonia-recycling enzyme was present in this compartment, potentially leaving more ammonia available for excretion. organism: Mus musculus tissue_or_cell_type: renal proximal tubule experimental_model: Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays. limitations: Expression and localization were measured; the quantitative contribution of GLUL to total flux was not isolated. experimental-exposure: Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays. endpoint: Diet-induced hypokalemia decreased glutamine synthetase expression throughout the mouse proximal tubule. [verlander-2013-gs] Expression of glutamine synthetase in the mouse kidney: localization in multiple epithelial cell types and differential regulation by hypokalemia (2013). https://pubmed.ncbi.nlm.nih.gov/23804452/ DOI: 10.1152/ajprenal.00030.2013
Complete structured claim and evidence
Renal mitochondria from potassium-depleted rats produced more ammonia during glutamine-metabolism assays after three days of potassium-free feeding.
Potassium → Renal ammonia production source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium depletion changes mitochondrial glutamine nitrogen metabolism; enzyme capacity and substrate entry need separate accounting.
endpoint
Renal mitochondria from potassium-depleted rats produced more ammonia during glutamine-metabolism assays after three days of potassium-free feeding.
experimental-exposure
Rats on potassium-free diet with renal mitochondrial and cortical-tubule ammonia assays during depletion and potassium refeeding.
experimental_model
Rats on potassium-free diet with renal mitochondrial and cortical-tubule ammonia assays during depletion and potassium refeeding.
limitations
Isolated mitochondrial assay, not whole-body bicarbonate balance. Glutaminase activity rose earlier than ammonia flux; mitochondrial glutamine entry was proposed as a limiting step.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
The kidney adaptation included greater ammonia production, beyond changes in enzyme abundance.
primary_references
[sastrasinh-1986-mitochondrial-ammonia] Renal mitochondrial glutamine metabolism during K+ depletion (1986). https://pubmed.ncbi.nlm.nih.gov/3963205/ DOI: 10.1152/ajprenal.1986.250.4.F667
tissue_or_cell_type
renal mitochondria
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1041–1053
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats on potassium-free diet with renal mitochondrial and cortical-tubule ammonia assays during depletion and potassium refeeding. · source_derived_draft · unverified_draft
### k-depletion-increases-mitochondrial-ammonia Renal mitochondria from potassium-depleted rats produced more ammonia during glutamine-metabolism assays after three days of potassium-free feeding. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidney adaptation included greater ammonia production, beyond changes in enzyme abundance. organism: Rattus norvegicus tissue_or_cell_type: renal mitochondria experimental_model: Rats on potassium-free diet with renal mitochondrial and cortical-tubule ammonia assays during depletion and potassium refeeding. limitations: Isolated mitochondrial assay, not whole-body bicarbonate balance. Glutaminase activity rose earlier than ammonia flux; mitochondrial glutamine entry was proposed as a limiting step. cross_nutrient: Potassium depletion changes mitochondrial glutamine nitrogen metabolism; enzyme capacity and substrate entry need separate accounting. experimental-exposure: Rats on potassium-free diet with renal mitochondrial and cortical-tubule ammonia assays during depletion and potassium refeeding. endpoint: Renal mitochondria from potassium-depleted rats produced more ammonia during glutamine-metabolism assays after three days of potassium-free feeding. [sastrasinh-1986-mitochondrial-ammonia] Renal mitochondrial glutamine metabolism during K+ depletion (1986). https://pubmed.ncbi.nlm.nih.gov/3963205/ DOI: 10.1152/ajprenal.1986.250.4.F667
Complete structured claim and evidence
The same hypokalemic diet increased glutamine synthetase expression in type A intercalated cells.
Potassium → Glutamine synthetase / GLUL source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
endpoint
The same hypokalemic diet increased glutamine synthetase expression in type A intercalated cells.
experimental-exposure
Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays.
experimental_model
Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays.
limitations
Cell-specific regulation is not a contradiction of the proximal-tubule result; neither establishes net flux in an intact human kidney.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
Different kidney cells adjusted the same ammonia-recycling enzyme in opposite directions.
primary_references
[verlander-2013-gs] Expression of glutamine synthetase in the mouse kidney: localization in multiple epithelial cell types and differential regulation by hypokalemia (2013). https://pubmed.ncbi.nlm.nih.gov/23804452/ DOI: 10.1152/ajprenal.00030.2013
tissue_or_cell_type
type A intercalated cells of cortical and outer medullary collecting duct
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1055–1066
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays. · source_derived_draft · unverified_draft
### k-depletion-intercalated-glul The same hypokalemic diet increased glutamine synthetase expression in type A intercalated cells. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different kidney cells adjusted the same ammonia-recycling enzyme in opposite directions. organism: Mus musculus tissue_or_cell_type: type A intercalated cells of cortical and outer medullary collecting duct experimental_model: Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays. limitations: Cell-specific regulation is not a contradiction of the proximal-tubule result; neither establishes net flux in an intact human kidney. experimental-exposure: Mice fed a nominally potassium-free diet for 12 days; renal immunolabeling and protein/RNA assays. endpoint: The same hypokalemic diet increased glutamine synthetase expression in type A intercalated cells. [verlander-2013-gs] Expression of glutamine synthetase in the mouse kidney: localization in multiple epithelial cell types and differential regulation by hypokalemia (2013). https://pubmed.ncbi.nlm.nih.gov/23804452/ DOI: 10.1152/ajprenal.00030.2013
Complete structured claim and evidence
Four days of potassium-free diet increased cortical proximal-tubule NBCe1-A expression in wild-type mice.
Potassium → NBCe1-A splice variant source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium deprivation regulates sodium-bicarbonate transport machinery.
endpoint
Four days of potassium-free diet increased cortical proximal-tubule NBCe1-A expression in wild-type mice.
experimental-exposure
NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response.
experimental_model
NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response.
limitations
Expression was measured; this record does not assign a bicarbonate transport stoichiometry or measure its flux.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
A sodium-bicarbonate transporter adapted during potassium conservation.
primary_references
[lee-2020-nbce1a] NBCe1-A is required for the renal ammonia and K+ response to hypokalemia (2020). https://pubmed.ncbi.nlm.nih.gov/31841393/ DOI: 10.1152/ajprenal.00481.2019
tissue_or_cell_type
cortical proximal tubule
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1068–1080
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response. · source_derived_draft · unverified_draft
### k-free-diet-increases-nbce1a Four days of potassium-free diet increased cortical proximal-tubule NBCe1-A expression in wild-type mice. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sodium-bicarbonate transporter adapted during potassium conservation. organism: Mus musculus tissue_or_cell_type: cortical proximal tubule experimental_model: NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response. limitations: Expression was measured; this record does not assign a bicarbonate transport stoichiometry or measure its flux. cross_nutrient: Potassium deprivation regulates sodium-bicarbonate transport machinery. experimental-exposure: NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response. endpoint: Four days of potassium-free diet increased cortical proximal-tubule NBCe1-A expression in wild-type mice. [lee-2020-nbce1a] NBCe1-A is required for the renal ammonia and K+ response to hypokalemia (2020). https://pubmed.ncbi.nlm.nih.gov/31841393/ DOI: 10.1152/ajprenal.00481.2019
Complete structured claim and evidence
NBCe1-A deletion blunted the urinary ammonia-excretion response to potassium-free feeding.
NBCe1-A splice variant → Urinary total ammonia excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
cross_nutrient
Sodium-bicarbonate transport machinery is required for the full potassium-responsive ammonia adaptation.
endpoint
NBCe1-A deletion blunted the urinary ammonia-excretion response to potassium-free feeding.
experimental-exposure
NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response.
experimental_model
NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response.
limitations
Assay reports total ammonia. Knockout also causes acidosis and outer-medullary compensation; the exact signal is unresolved.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
A sodium-bicarbonate transporter was needed for the full kidney ammonia response to potassium deprivation.
primary_references
[lee-2020-nbce1a] NBCe1-A is required for the renal ammonia and K+ response to hypokalemia (2020). https://pubmed.ncbi.nlm.nih.gov/31841393/ DOI: 10.1152/ajprenal.00481.2019
tissue_or_cell_type
cortical proximal tubule and urinary ammonia output
trigger_kind
machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1082–1094
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response. · source_derived_draft · unverified_draft
### nbce1a-loss-blunts-k-ammonia-response NBCe1-A deletion blunted the urinary ammonia-excretion response to potassium-free feeding. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sodium-bicarbonate transporter was needed for the full kidney ammonia response to potassium deprivation. organism: Mus musculus tissue_or_cell_type: cortical proximal tubule and urinary ammonia output experimental_model: NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response. limitations: Assay reports total ammonia. Knockout also causes acidosis and outer-medullary compensation; the exact signal is unresolved. cross_nutrient: Sodium-bicarbonate transport machinery is required for the full potassium-responsive ammonia adaptation. experimental-exposure: NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response. endpoint: NBCe1-A deletion blunted the urinary ammonia-excretion response to potassium-free feeding. [lee-2020-nbce1a] NBCe1-A is required for the renal ammonia and K+ response to hypokalemia (2020). https://pubmed.ncbi.nlm.nih.gov/31841393/ DOI: 10.1152/ajprenal.00481.2019
Complete structured claim and evidence
Luminal omeprazole abolished net total-CO2 flux used to measure acidification in collecting ducts from potassium-restricted rabbits.
Renal hydrogen-potassium ATPase activities → Collecting duct proton secretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
endpoint
Luminal omeprazole abolished net total-CO2 flux used to measure acidification in collecting ducts from potassium-restricted rabbits.
experimental-exposure
Microperfused inner-stripe outer medullary collecting ducts from rabbits fed 0.55% potassium diet for 7-14 days; luminal omeprazole 0.1 mM.
experimental_model
Microperfused inner-stripe outer medullary collecting ducts from rabbits fed 0.55% potassium diet for 7-14 days; luminal omeprazole 0.1 mM.
limitations
Pharmacological activity assignment; the experiment does not isolate ATP4A versus ATP12A. Total-CO2 flux is an acidification surrogate.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Oryctolagus cuniculus
plain_language
An H/K-pump-compatible activity supported acid secretion in the isolated duct.
primary_references
[wingo-1989-hka] Active proton secretion and potassium absorption in the rabbit outer medullary collecting duct. Functional evidence for proton-potassium-activated adenosine triphosphatase (1989). https://pubmed.ncbi.nlm.nih.gov/2544629/ DOI: 10.1172/JCI114165
tissue_or_cell_type
inner-stripe outer medullary collecting duct
transport_direction
potassium: tubular lumen toward blood; protons: cell toward tubular lumen
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1096–1108
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Microperfused inner-stripe outer medullary collecting ducts from rabbits fed 0.55% potassium diet for 7-14 days; luminal omeprazole 0.1 mM. · source_derived_draft · unverified_draft
### hka-sensitive-proton-secretion Luminal omeprazole abolished net total-CO2 flux used to measure acidification in collecting ducts from potassium-restricted rabbits. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An H/K-pump-compatible activity supported acid secretion in the isolated duct. organism: Oryctolagus cuniculus tissue_or_cell_type: inner-stripe outer medullary collecting duct experimental_model: Microperfused inner-stripe outer medullary collecting ducts from rabbits fed 0.55% potassium diet for 7-14 days; luminal omeprazole 0.1 mM. limitations: Pharmacological activity assignment; the experiment does not isolate ATP4A versus ATP12A. Total-CO2 flux is an acidification surrogate. transport_direction: potassium: tubular lumen toward blood; protons: cell toward tubular lumen experimental-exposure: Microperfused inner-stripe outer medullary collecting ducts from rabbits fed 0.55% potassium diet for 7-14 days; luminal omeprazole 0.1 mM. endpoint: Luminal omeprazole abolished net total-CO2 flux used to measure acidification in collecting ducts from potassium-restricted rabbits. [wingo-1989-hka] Active proton secretion and potassium absorption in the rabbit outer medullary collecting duct. Functional evidence for proton-potassium-activated adenosine triphosphatase (1989). https://pubmed.ncbi.nlm.nih.gov/2544629/ DOI: 10.1172/JCI114165
Complete structured claim and evidence
Luminal omeprazole abolished active net potassium absorption in the same potassium-restricted rabbit collecting-duct preparation.
Renal hydrogen-potassium ATPase activities → Collecting duct potassium reabsorption source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
endpoint
Luminal omeprazole abolished active net potassium absorption in the same potassium-restricted rabbit collecting-duct preparation.
experimental-exposure
Microperfused inner-stripe outer medullary collecting ducts from rabbits fed 0.55% potassium diet for 7-14 days; luminal omeprazole 0.1 mM.
experimental_model
Microperfused inner-stripe outer medullary collecting ducts from rabbits fed 0.55% potassium diet for 7-14 days; luminal omeprazole 0.1 mM.
limitations
Pharmacological activity assignment; the experiment does not isolate ATP4A versus ATP12A. Total-CO2 flux is an acidification surrogate.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Oryctolagus cuniculus
plain_language
The proton-pump-compatible activity also recovered potassium from tubular fluid.
primary_references
[wingo-1989-hka] Active proton secretion and potassium absorption in the rabbit outer medullary collecting duct. Functional evidence for proton-potassium-activated adenosine triphosphatase (1989). https://pubmed.ncbi.nlm.nih.gov/2544629/ DOI: 10.1172/JCI114165
tissue_or_cell_type
inner-stripe outer medullary collecting duct
transport_direction
potassium: tubular lumen toward blood; protons: cell toward tubular lumen
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1110–1122
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Microperfused inner-stripe outer medullary collecting ducts from rabbits fed 0.55% potassium diet for 7-14 days; luminal omeprazole 0.1 mM. · source_derived_draft · unverified_draft
### hka-sensitive-potassium-absorption Luminal omeprazole abolished active net potassium absorption in the same potassium-restricted rabbit collecting-duct preparation. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The proton-pump-compatible activity also recovered potassium from tubular fluid. organism: Oryctolagus cuniculus tissue_or_cell_type: inner-stripe outer medullary collecting duct experimental_model: Microperfused inner-stripe outer medullary collecting ducts from rabbits fed 0.55% potassium diet for 7-14 days; luminal omeprazole 0.1 mM. limitations: Pharmacological activity assignment; the experiment does not isolate ATP4A versus ATP12A. Total-CO2 flux is an acidification surrogate. transport_direction: potassium: tubular lumen toward blood; protons: cell toward tubular lumen experimental-exposure: Microperfused inner-stripe outer medullary collecting ducts from rabbits fed 0.55% potassium diet for 7-14 days; luminal omeprazole 0.1 mM. endpoint: Luminal omeprazole abolished active net potassium absorption in the same potassium-restricted rabbit collecting-duct preparation. [wingo-1989-hka] Active proton secretion and potassium absorption in the rabbit outer medullary collecting duct. Functional evidence for proton-potassium-activated adenosine triphosphatase (1989). https://pubmed.ncbi.nlm.nih.gov/2544629/ DOI: 10.1172/JCI114165
Complete structured claim and evidence
Potassium depletion increased collecting-tubule potassium-stimulated, ouabain-insensitive ATPase activity in rats.
Potassium → Renal hydrogen-potassium ATPase activities source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
endpoint
Potassium depletion increased collecting-tubule potassium-stimulated, ouabain-insensitive ATPase activity in rats.
experimental-exposure
Microdissected rabbit nephron segments and collecting tubules of potassium-depleted rats.
experimental_model
Microdissected rabbit nephron segments and collecting tubules of potassium-depleted rats.
limitations
ATP hydrolysis and inhibitor sensitivity establish activity class, not a specific protein isoform or whole-animal flux.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
The distal kidney increased an ATP-consuming activity compatible with potassium recovery.
primary_references
[doucet-1987-hka] Characterization of K-ATPase activity in distal nephron: stimulation by potassium depletion (1987). https://pubmed.ncbi.nlm.nih.gov/2957926/ DOI: 10.1152/ajprenal.1987.253.3.F418
tissue_or_cell_type
collecting tubule
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1124–1135
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Microdissected rabbit nephron segments and collecting tubules of potassium-depleted rats. · source_derived_draft · unverified_draft
### k-depletion-increases-hka-activity Potassium depletion increased collecting-tubule potassium-stimulated, ouabain-insensitive ATPase activity in rats. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The distal kidney increased an ATP-consuming activity compatible with potassium recovery. organism: Rattus norvegicus tissue_or_cell_type: collecting tubule experimental_model: Microdissected rabbit nephron segments and collecting tubules of potassium-depleted rats. limitations: ATP hydrolysis and inhibitor sensitivity establish activity class, not a specific protein isoform or whole-animal flux. experimental-exposure: Microdissected rabbit nephron segments and collecting tubules of potassium-depleted rats. endpoint: Potassium depletion increased collecting-tubule potassium-stimulated, ouabain-insensitive ATPase activity in rats. [doucet-1987-hka] Characterization of K-ATPase activity in distal nephron: stimulation by potassium depletion (1987). https://pubmed.ncbi.nlm.nih.gov/2957926/ DOI: 10.1152/ajprenal.1987.253.3.F418
Complete structured claim and evidence
In adrenalectomized rats, low potassium combined with high aldosterone produced a larger serum-bicarbonate rise than either perturbation alone.
Potassium → Bicarbonate ion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium and aldosterone-dependent sodium/acid handling jointly influence systemic bicarbonate.
endpoint
In adrenalectomized rats, low potassium combined with high aldosterone produced a larger serum-bicarbonate rise than either perturbation alone.
experimental-exposure
Glucocorticoid-replete adrenalectomized rats with varied dietary potassium and zero, physiological, or pharmacological aldosterone replacement.
experimental_model
Glucocorticoid-replete adrenalectomized rats with varied dietary potassium and zero, physiological, or pharmacological aldosterone replacement.
limitations
Endocrine replacement experiment, not ordinary dietary deficiency; H/K-ATPase and H-ATPase were regulated differently.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
Potassium depletion and mineralocorticoid exposure can act together on renal acid handling.
primary_references
[eiam-1993-atpases] Regulation of collecting tubule adenosine triphosphatases by aldosterone and potassium (1993). https://pubmed.ncbi.nlm.nih.gov/8390478/ DOI: 10.1172/JCI116471
tissue_or_cell_type
collecting tubule and systemic blood
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1137–1149
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Glucocorticoid-replete adrenalectomized rats with varied dietary potassium and zero, physiological, or pharmacological aldosterone replacement. · source_derived_draft · unverified_draft
### k-aldosterone-joint-bicarbonate In adrenalectomized rats, low potassium combined with high aldosterone produced a larger serum-bicarbonate rise than either perturbation alone. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium depletion and mineralocorticoid exposure can act together on renal acid handling. organism: Rattus norvegicus tissue_or_cell_type: collecting tubule and systemic blood experimental_model: Glucocorticoid-replete adrenalectomized rats with varied dietary potassium and zero, physiological, or pharmacological aldosterone replacement. limitations: Endocrine replacement experiment, not ordinary dietary deficiency; H/K-ATPase and H-ATPase were regulated differently. cross_nutrient: Potassium and aldosterone-dependent sodium/acid handling jointly influence systemic bicarbonate. experimental-exposure: Glucocorticoid-replete adrenalectomized rats with varied dietary potassium and zero, physiological, or pharmacological aldosterone replacement. endpoint: In adrenalectomized rats, low potassium combined with high aldosterone produced a larger serum-bicarbonate rise than either perturbation alone. [eiam-1993-atpases] Regulation of collecting tubule adenosine triphosphatases by aldosterone and potassium (1993). https://pubmed.ncbi.nlm.nih.gov/8390478/ DOI: 10.1172/JCI116471
Complete structured claim and evidence
HCl infusion causing acute mineral acidemia raised plasma potassium in the conscious-dog experiment.
Hydrochloric acid → Serum or plasma potassium concentration source_derived_draftungraded
Experimental context and source evidence
endpoint
HCl infusion causing acute mineral acidemia raised plasma potassium in the conscious-dog experiment.
experimental-exposure
Experimental acute mineral acidemia with hyperkalemia; not potassium deficiency or excessive potassium intake.
experimental_model
Twelve conscious dogs with portal/hepatic/systemic sampling; beta-hydroxybutyric acid 7 mEq/kg or HCl 3 mEq/kg infused over 30 minutes; additional anesthetized and obstructed-urinary-tract studies.
limitations
Acute HCl infusion, not every acidosis; portal glucagon rose and direct H/K exchange was not isolated.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Canis lupus familiaris
plain_language
Acid type affected the potassium response; a rise in blood potassium did not imply excess potassium intake.
primary_references
[adrogue-1985-acid-infusion] Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs (1985). https://www.jci.org/articles/view/111775 DOI: 10.1172/JCI111775
tissue_or_cell_type
systemic and splanchnic circulation
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1151–1162
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twelve conscious dogs with portal/hepatic/systemic sampling; beta-hydroxybutyric acid 7 mEq/kg or HCl 3 mEq/kg infused over 30 minutes; additional anesthetized and obstructed-urinary-tract studies. · source_derived_draft · unverified_draft
### hcl-acidemia-raises-plasma-k HCl infusion causing acute mineral acidemia raised plasma potassium in the conscious-dog experiment. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Acid type affected the potassium response; a rise in blood potassium did not imply excess potassium intake. organism: Canis lupus familiaris tissue_or_cell_type: systemic and splanchnic circulation experimental_model: Twelve conscious dogs with portal/hepatic/systemic sampling; beta-hydroxybutyric acid 7 mEq/kg or HCl 3 mEq/kg infused over 30 minutes; additional anesthetized and obstructed-urinary-tract studies. limitations: Acute HCl infusion, not every acidosis; portal glucagon rose and direct H/K exchange was not isolated. experimental-exposure: Experimental acute mineral acidemia with hyperkalemia; not potassium deficiency or excessive potassium intake. endpoint: HCl infusion causing acute mineral acidemia raised plasma potassium in the conscious-dog experiment. [adrogue-1985-acid-infusion] Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs (1985). https://www.jci.org/articles/view/111775 DOI: 10.1172/JCI111775
Complete structured claim and evidence
Beta-hydroxybutyric acid infusion increased portal insulin in conscious dogs.
Beta-hydroxybutyric acid → Insulin source_derived_draftungraded
Experimental context and source evidence
endpoint
Beta-hydroxybutyric acid infusion increased portal insulin in conscious dogs.
experimental-exposure
Twelve conscious dogs with portal/hepatic/systemic sampling; beta-hydroxybutyric acid 7 mEq/kg or HCl 3 mEq/kg infused over 30 minutes; additional anesthetized and obstructed-urinary-tract studies.
experimental_model
Twelve conscious dogs with portal/hepatic/systemic sampling; beta-hydroxybutyric acid 7 mEq/kg or HCl 3 mEq/kg infused over 30 minutes; additional anesthetized and obstructed-urinary-tract studies.
limitations
Racemic ketone-acid infusion into nondiabetic animals does not model insulin-deficient diabetic ketoacidosis.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Canis lupus familiaris
plain_language
The ketone-acid intervention changed the hormone environment that controls potassium distribution.
primary_references
[adrogue-1985-acid-infusion] Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs (1985). https://www.jci.org/articles/view/111775 DOI: 10.1172/JCI111775
tissue_or_cell_type
pancreatic-portal circulation
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1164–1175
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twelve conscious dogs with portal/hepatic/systemic sampling; beta-hydroxybutyric acid 7 mEq/kg or HCl 3 mEq/kg infused over 30 minutes; additional anesthetized and obstructed-urinary-tract studies. · source_derived_draft · unverified_draft
### ketoacid-infusion-raises-portal-insulin Beta-hydroxybutyric acid infusion increased portal insulin in conscious dogs. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The ketone-acid intervention changed the hormone environment that controls potassium distribution. organism: Canis lupus familiaris tissue_or_cell_type: pancreatic-portal circulation experimental_model: Twelve conscious dogs with portal/hepatic/systemic sampling; beta-hydroxybutyric acid 7 mEq/kg or HCl 3 mEq/kg infused over 30 minutes; additional anesthetized and obstructed-urinary-tract studies. limitations: Racemic ketone-acid infusion into nondiabetic animals does not model insulin-deficient diabetic ketoacidosis. experimental-exposure: Twelve conscious dogs with portal/hepatic/systemic sampling; beta-hydroxybutyric acid 7 mEq/kg or HCl 3 mEq/kg infused over 30 minutes; additional anesthetized and obstructed-urinary-tract studies. endpoint: Beta-hydroxybutyric acid infusion increased portal insulin in conscious dogs. [adrogue-1985-acid-infusion] Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs (1985). https://www.jci.org/articles/view/111775 DOI: 10.1172/JCI111775
Complete structured claim and evidence
Beta-hydroxybutyric acid infusion lowered plasma potassium despite acidemia comparable to the HCl intervention.
Beta-hydroxybutyric acid → Serum or plasma potassium concentration source_derived_draftungraded
Experimental context and source evidence
endpoint
Beta-hydroxybutyric acid infusion lowered plasma potassium despite acidemia comparable to the HCl intervention.
experimental-exposure
Acute ketone-acid infusion with intact endocrine pancreas; redistribution-associated hypokalemia, not nutritional potassium depletion.
experimental_model
Twelve conscious dogs with portal/hepatic/systemic sampling; beta-hydroxybutyric acid 7 mEq/kg or HCl 3 mEq/kg infused over 30 minutes; additional anesthetized and obstructed-urinary-tract studies.
limitations
Redistribution is supported by renal-excretion controls; hepatic uptake and hormonal causation were proposed, not definitively localized. Other organic acids were untested.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Canis lupus familiaris
plain_language
Acidemia alone did not predict the direction of blood potassium change.
primary_references
[adrogue-1985-acid-infusion] Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs (1985). https://www.jci.org/articles/view/111775 DOI: 10.1172/JCI111775
tissue_or_cell_type
systemic circulation
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1177–1188
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twelve conscious dogs with portal/hepatic/systemic sampling; beta-hydroxybutyric acid 7 mEq/kg or HCl 3 mEq/kg infused over 30 minutes; additional anesthetized and obstructed-urinary-tract studies. · source_derived_draft · unverified_draft
### ketoacid-infusion-lowers-plasma-k Beta-hydroxybutyric acid infusion lowered plasma potassium despite acidemia comparable to the HCl intervention. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Acidemia alone did not predict the direction of blood potassium change. organism: Canis lupus familiaris tissue_or_cell_type: systemic circulation experimental_model: Twelve conscious dogs with portal/hepatic/systemic sampling; beta-hydroxybutyric acid 7 mEq/kg or HCl 3 mEq/kg infused over 30 minutes; additional anesthetized and obstructed-urinary-tract studies. limitations: Redistribution is supported by renal-excretion controls; hepatic uptake and hormonal causation were proposed, not definitively localized. Other organic acids were untested. experimental-exposure: Acute ketone-acid infusion with intact endocrine pancreas; redistribution-associated hypokalemia, not nutritional potassium depletion. endpoint: Beta-hydroxybutyric acid infusion lowered plasma potassium despite acidemia comparable to the HCl intervention. [adrogue-1985-acid-infusion] Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs (1985). https://www.jci.org/articles/view/111775 DOI: 10.1172/JCI111775
Complete structured claim and evidence
Fourteen days of potassium depletion increased maximal sodium-dependent citrate transport in rat renal brush-border vesicles.
Potassium → Renal apical sodium-citrate cotransport source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium depletion regulates a sodium-dependent organic-anion transport process relevant to calcium-stone chemistry.
endpoint
Fourteen days of potassium depletion increased maximal sodium-dependent citrate transport in rat renal brush-border vesicles.
experimental-exposure
Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics.
experimental_model
Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics.
limitations
Vesicle transport capacity is not a direct in-vivo flux measurement; molecular isoform identity was not tested.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
The proximal-tubule uptake system could reclaim citrate faster, linking potassium depletion to sodium-coupled citrate handling.
primary_references
[levi-1991-citrate] Chronic K depletion stimulates rat renal brush-border membrane Na-citrate cotransporter (1991). https://pubmed.ncbi.nlm.nih.gov/1683169/ DOI: 10.1152/ajprenal.1991.261.5.F767
tissue_or_cell_type
renal proximal-tubule apical membrane
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1190–1202
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics. · source_derived_draft · unverified_draft
### k-depletion-increases-na-citrate-transport Fourteen days of potassium depletion increased maximal sodium-dependent citrate transport in rat renal brush-border vesicles. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The proximal-tubule uptake system could reclaim citrate faster, linking potassium depletion to sodium-coupled citrate handling. organism: Rattus norvegicus tissue_or_cell_type: renal proximal-tubule apical membrane experimental_model: Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics. limitations: Vesicle transport capacity is not a direct in-vivo flux measurement; molecular isoform identity was not tested. cross_nutrient: Potassium depletion regulates a sodium-dependent organic-anion transport process relevant to calcium-stone chemistry. experimental-exposure: Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics. endpoint: Fourteen days of potassium depletion increased maximal sodium-dependent citrate transport in rat renal brush-border vesicles. [levi-1991-citrate] Chronic K depletion stimulates rat renal brush-border membrane Na-citrate cotransporter (1991). https://pubmed.ncbi.nlm.nih.gov/1683169/ DOI: 10.1152/ajprenal.1991.261.5.F767
Complete structured claim and evidence
The potassium-depleted rats had reduced fractional urinary citrate excretion.
Potassium → Urinary citrate excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Citrate affects urinary calcium chemistry, but this depletion experiment measured citrate handling rather than stones.
endpoint
The potassium-depleted rats had reduced fractional urinary citrate excretion.
experimental-exposure
Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics.
experimental_model
Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics.
limitations
The transport and excretion measurements were parallel; downstream stone formation was not tested.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
Less filtered citrate remained in urine during depletion.
primary_references
[levi-1991-citrate] Chronic K depletion stimulates rat renal brush-border membrane Na-citrate cotransporter (1991). https://pubmed.ncbi.nlm.nih.gov/1683169/ DOI: 10.1152/ajprenal.1991.261.5.F767
tissue_or_cell_type
kidney and urine
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1204–1216
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics. · source_derived_draft · unverified_draft
### k-depletion-lowers-citrate-excretion The potassium-depleted rats had reduced fractional urinary citrate excretion. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less filtered citrate remained in urine during depletion. organism: Rattus norvegicus tissue_or_cell_type: kidney and urine experimental_model: Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics. limitations: The transport and excretion measurements were parallel; downstream stone formation was not tested. cross_nutrient: Citrate affects urinary calcium chemistry, but this depletion experiment measured citrate handling rather than stones. experimental-exposure: Rats given low-potassium diet for 14 days; urine citrate and renal cortical brush-border membrane vesicle transport kinetics. endpoint: The potassium-depleted rats had reduced fractional urinary citrate excretion. [levi-1991-citrate] Chronic K depletion stimulates rat renal brush-border membrane Na-citrate cotransporter (1991). https://pubmed.ncbi.nlm.nih.gov/1683169/ DOI: 10.1152/ajprenal.1991.261.5.F767
Complete structured claim and evidence
Potassium citrate increased urine citrate excretion and clearance in the small stone-patient comparison.
Potassium citrate → Urinary citrate excretion source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Potassium-salt anion determines effects on urinary citrate, which participates in calcium complexation.
endpoint
Potassium citrate increased urine citrate excretion and clearance in the small stone-patient comparison.
experimental-exposure
Eight patients with stones, without potassium deficiency, compared after two weeks of potassium citrate, bicarbonate, or chloride at 80 mEq/day.
experimental_model
Eight patients with stones, without potassium deficiency, compared after two weeks of potassium citrate, bicarbonate, or chloride at 80 mEq/day.
limitations
Eight patients, short intervention; absence of potassium deficiency limits extrapolation to depletion. Alkali and citrate coeffects cannot be assigned to potassium cation alone.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
This salt raised citrate availability in urine, with accompanying alkali delivery.
primary_references
[sakhaee-1991-salts] Contrasting effects of various potassium salts on renal citrate excretion (1991). https://pubmed.ncbi.nlm.nih.gov/1899422/ DOI: 10.1210/jcem-72-2-396
tissue_or_cell_type
kidney and urine
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1218–1230
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Eight patients with stones, without potassium deficiency, compared after two weeks of potassium citrate, bicarbonate, or chloride at 80 mEq/day. · source_derived_draft · unverified_draft
### kcitrate-increases-urine-citrate Potassium citrate increased urine citrate excretion and clearance in the small stone-patient comparison. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This salt raised citrate availability in urine, with accompanying alkali delivery. organism: Homo sapiens tissue_or_cell_type: kidney and urine experimental_model: Eight patients with stones, without potassium deficiency, compared after two weeks of potassium citrate, bicarbonate, or chloride at 80 mEq/day. limitations: Eight patients, short intervention; absence of potassium deficiency limits extrapolation to depletion. Alkali and citrate coeffects cannot be assigned to potassium cation alone. cross_nutrient: Potassium-salt anion determines effects on urinary citrate, which participates in calcium complexation. experimental-exposure: Eight patients with stones, without potassium deficiency, compared after two weeks of potassium citrate, bicarbonate, or chloride at 80 mEq/day. endpoint: Potassium citrate increased urine citrate excretion and clearance in the small stone-patient comparison. [sakhaee-1991-salts] Contrasting effects of various potassium salts on renal citrate excretion (1991). https://pubmed.ncbi.nlm.nih.gov/1899422/ DOI: 10.1210/jcem-72-2-396
Complete structured claim and evidence
Potassium bicarbonate increased urine citrate excretion and clearance in the same comparison.
Potassium bicarbonate → Urinary citrate excretion source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Potassium-salt anion determines effects on urinary citrate, which participates in calcium complexation.
endpoint
Potassium bicarbonate increased urine citrate excretion and clearance in the same comparison.
experimental-exposure
Eight patients with stones, without potassium deficiency, compared after two weeks of potassium citrate, bicarbonate, or chloride at 80 mEq/day.
experimental_model
Eight patients with stones, without potassium deficiency, compared after two weeks of potassium citrate, bicarbonate, or chloride at 80 mEq/day.
limitations
Eight patients, short intervention; absence of potassium deficiency limits extrapolation to depletion. Alkali and citrate coeffects cannot be assigned to potassium cation alone.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
An alkali salt without administered citrate reproduced the citraturic response.
primary_references
[sakhaee-1991-salts] Contrasting effects of various potassium salts on renal citrate excretion (1991). https://pubmed.ncbi.nlm.nih.gov/1899422/ DOI: 10.1210/jcem-72-2-396
tissue_or_cell_type
kidney and urine
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1232–1244
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Eight patients with stones, without potassium deficiency, compared after two weeks of potassium citrate, bicarbonate, or chloride at 80 mEq/day. · source_derived_draft · unverified_draft
### kbicarbonate-increases-urine-citrate Potassium bicarbonate increased urine citrate excretion and clearance in the same comparison. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An alkali salt without administered citrate reproduced the citraturic response. organism: Homo sapiens tissue_or_cell_type: kidney and urine experimental_model: Eight patients with stones, without potassium deficiency, compared after two weeks of potassium citrate, bicarbonate, or chloride at 80 mEq/day. limitations: Eight patients, short intervention; absence of potassium deficiency limits extrapolation to depletion. Alkali and citrate coeffects cannot be assigned to potassium cation alone. cross_nutrient: Potassium-salt anion determines effects on urinary citrate, which participates in calcium complexation. experimental-exposure: Eight patients with stones, without potassium deficiency, compared after two weeks of potassium citrate, bicarbonate, or chloride at 80 mEq/day. endpoint: Potassium bicarbonate increased urine citrate excretion and clearance in the same comparison. [sakhaee-1991-salts] Contrasting effects of various potassium salts on renal citrate excretion (1991). https://pubmed.ncbi.nlm.nih.gov/1899422/ DOI: 10.1210/jcem-72-2-396
Complete structured claim and evidence
Potassium chloride did not significantly raise urinary citrate in these participants without potassium deficiency.
Potassium chloride → Urinary citrate excretion source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Potassium-salt anion determines effects on urinary citrate, which participates in calcium complexation.
endpoint
Potassium chloride did not significantly raise urinary citrate in these participants without potassium deficiency.
experimental-exposure
Eight patients with stones, without potassium deficiency, compared after two weeks of potassium citrate, bicarbonate, or chloride at 80 mEq/day.
experimental_model
Eight patients with stones, without potassium deficiency, compared after two weeks of potassium citrate, bicarbonate, or chloride at 80 mEq/day.
limitations
Eight patients, short intervention; absence of potassium deficiency limits extrapolation to depletion. Alkali and citrate coeffects cannot be assigned to potassium cation alone.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
Additional potassium without alkali did not reproduce the citrate response in this group.
primary_references
[sakhaee-1991-salts] Contrasting effects of various potassium salts on renal citrate excretion (1991). https://pubmed.ncbi.nlm.nih.gov/1899422/ DOI: 10.1210/jcem-72-2-396
tissue_or_cell_type
kidney and urine
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1246–1258
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Eight patients with stones, without potassium deficiency, compared after two weeks of potassium citrate, bicarbonate, or chloride at 80 mEq/day. · source_derived_draft · unverified_draft
### kchloride-no-citraturia-nondepleted Potassium chloride did not significantly raise urinary citrate in these participants without potassium deficiency. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Additional potassium without alkali did not reproduce the citrate response in this group. organism: Homo sapiens tissue_or_cell_type: kidney and urine experimental_model: Eight patients with stones, without potassium deficiency, compared after two weeks of potassium citrate, bicarbonate, or chloride at 80 mEq/day. limitations: Eight patients, short intervention; absence of potassium deficiency limits extrapolation to depletion. Alkali and citrate coeffects cannot be assigned to potassium cation alone. cross_nutrient: Potassium-salt anion determines effects on urinary citrate, which participates in calcium complexation. experimental-exposure: Eight patients with stones, without potassium deficiency, compared after two weeks of potassium citrate, bicarbonate, or chloride at 80 mEq/day. endpoint: Potassium chloride did not significantly raise urinary citrate in these participants without potassium deficiency. [sakhaee-1991-salts] Contrasting effects of various potassium salts on renal citrate excretion (1991). https://pubmed.ncbi.nlm.nih.gov/1899422/ DOI: 10.1210/jcem-72-2-396
Complete structured claim and evidence
The bicarbonate-containing arms reduced calcium excretion relative to non-bicarbonate arms in the older-adult trial; a potassium main effect was not significant.
Bicarbonate ion → Urinary calcium excretion source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Bicarbonate coadministration modifies the calcium response attributed to potassium salts.
endpoint
The bicarbonate-containing arms reduced calcium excretion relative to non-bicarbonate arms in the older-adult trial; a potassium main effect was not significant.
experimental-exposure
171 adults aged at least 50 randomized to placebo, KHCO3, NaHCO3, or KCl at 67.5 mmol/day for three months; 162 analyzed; all received calcium and vitamin D.
experimental_model
171 adults aged at least 50 randomized to placebo, KHCO3, NaHCO3, or KCl at 67.5 mmol/day for three months; 162 analyzed; all received calcium and vitamin D.
limitations
Pooled factorial comparison, calcium/vitamin D co-supplementation, three-month surrogate endpoint; not evidence of fracture prevention or universal potassium neutrality.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
The calcium-loss effect tracked the alkali component rather than the presence of potassium in the salt.
primary_references
[dawson-hughes-2009-bicarbonate] Treatment with Potassium Bicarbonate Lowers Calcium Excretion and Bone Resorption in Older Men and Women (2009). https://pmc.ncbi.nlm.nih.gov/articles/PMC2630872/ DOI: 10.1210/jc.2008-1662
tissue_or_cell_type
kidney and urine
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1260–1272
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 171 adults aged at least 50 randomized to placebo, KHCO3, NaHCO3, or KCl at 67.5 mmol/day for three months; 162 analyzed; all received calcium and vitamin D. · source_derived_draft · unverified_draft
### bicarbonate-component-lowers-calciuria The bicarbonate-containing arms reduced calcium excretion relative to non-bicarbonate arms in the older-adult trial; a potassium main effect was not significant. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The calcium-loss effect tracked the alkali component rather than the presence of potassium in the salt. organism: Homo sapiens tissue_or_cell_type: kidney and urine experimental_model: 171 adults aged at least 50 randomized to placebo, KHCO3, NaHCO3, or KCl at 67.5 mmol/day for three months; 162 analyzed; all received calcium and vitamin D. limitations: Pooled factorial comparison, calcium/vitamin D co-supplementation, three-month surrogate endpoint; not evidence of fracture prevention or universal potassium neutrality. cross_nutrient: Bicarbonate coadministration modifies the calcium response attributed to potassium salts. experimental-exposure: 171 adults aged at least 50 randomized to placebo, KHCO3, NaHCO3, or KCl at 67.5 mmol/day for three months; 162 analyzed; all received calcium and vitamin D. endpoint: The bicarbonate-containing arms reduced calcium excretion relative to non-bicarbonate arms in the older-adult trial; a potassium main effect was not significant. [dawson-hughes-2009-bicarbonate] Treatment with Potassium Bicarbonate Lowers Calcium Excretion and Bone Resorption in Older Men and Women (2009). https://pmc.ncbi.nlm.nih.gov/articles/PMC2630872/ DOI: 10.1210/jc.2008-1662
Complete structured claim and evidence
Five-day dietary potassium withdrawal increased fasting and daily urinary calcium excretion whether the withdrawn salt was KCl or KHCO3.
Potassium → Urinary calcium excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium deprivation increases renal calcium loss in a controlled human dietary model.
endpoint
Five-day dietary potassium withdrawal increased fasting and daily urinary calcium excretion whether the withdrawn salt was KCl or KHCO3.
experimental-exposure
Healthy adults on controlled diets; salt loading in ten participants and five-day potassium deprivation with recovery in two groups of four.
experimental_model
Healthy adults on controlled diets; salt loading in ten participants and five-day potassium deprivation with recovery in two groups of four.
limitations
Small controlled metabolic study; sodium balance, extracellular volume, phosphate handling and calcitriol were possible mediators rather than proven causal links.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
Potassium deprivation changed calcium retention even when alkali withdrawal was not the only explanation.
primary_references
[lemann-1991-calciuria] Potassium administration reduces and potassium deprivation increases urinary calcium excretion in healthy adults [corrected] (1991). https://pubmed.ncbi.nlm.nih.gov/1648646/ DOI: 10.1038/ki.1991.123
tissue_or_cell_type
kidney and urine
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1274–1286
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Healthy adults on controlled diets; salt loading in ten participants and five-day potassium deprivation with recovery in two groups of four. · source_derived_draft · unverified_draft
### human-k-withdrawal-increases-calciuria Five-day dietary potassium withdrawal increased fasting and daily urinary calcium excretion whether the withdrawn salt was KCl or KHCO3. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium deprivation changed calcium retention even when alkali withdrawal was not the only explanation. organism: Homo sapiens tissue_or_cell_type: kidney and urine experimental_model: Healthy adults on controlled diets; salt loading in ten participants and five-day potassium deprivation with recovery in two groups of four. limitations: Small controlled metabolic study; sodium balance, extracellular volume, phosphate handling and calcitriol were possible mediators rather than proven causal links. cross_nutrient: Potassium deprivation increases renal calcium loss in a controlled human dietary model. experimental-exposure: Healthy adults on controlled diets; salt loading in ten participants and five-day potassium deprivation with recovery in two groups of four. endpoint: Five-day dietary potassium withdrawal increased fasting and daily urinary calcium excretion whether the withdrawn salt was KCl or KHCO3. [lemann-1991-calciuria] Potassium administration reduces and potassium deprivation increases urinary calcium excretion in healthy adults [corrected] (1991). https://pubmed.ncbi.nlm.nih.gov/1648646/ DOI: 10.1038/ki.1991.123
Complete structured claim and evidence
Dietary potassium restriction increased urinary calcium excretion in the male-mouse experiments.
Potassium → Urinary calcium excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently.
endpoint
Dietary potassium restriction increased urinary calcium excretion in the male-mouse experiments.
experimental-exposure
Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.
experimental_model
Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.
limitations
Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
The kidneys lost more calcium when dietary potassium was restricted.
primary_references
[murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339
tissue_or_cell_type
kidney, blood and trabecular skeleton
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1288–1300
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. · source_derived_draft · unverified_draft
### mouse-k-restriction-calciuria Dietary potassium restriction increased urinary calcium excretion in the male-mouse experiments. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kidneys lost more calcium when dietary potassium was restricted. organism: Mus musculus tissue_or_cell_type: kidney, blood and trabecular skeleton experimental_model: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. limitations: Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated. cross_nutrient: Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently. experimental-exposure: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. endpoint: Dietary potassium restriction increased urinary calcium excretion in the male-mouse experiments. [murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339
Complete structured claim and evidence
Dietary potassium restriction reduced measured plasma total calcium in the male mice.
Potassium → Serum total calcium concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently.
endpoint
Dietary potassium restriction reduced measured plasma total calcium in the male mice.
experimental-exposure
Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.
experimental_model
Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.
limitations
Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
Blood total calcium fell alongside increased urinary calcium loss.
primary_references
[murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339
tissue_or_cell_type
kidney, blood and trabecular skeleton
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1302–1314
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. · source_derived_draft · unverified_draft
### mouse-k-restriction-low-calcium Dietary potassium restriction reduced measured plasma total calcium in the male mice. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blood total calcium fell alongside increased urinary calcium loss. organism: Mus musculus tissue_or_cell_type: kidney, blood and trabecular skeleton experimental_model: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. limitations: Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated. cross_nutrient: Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently. experimental-exposure: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. endpoint: Dietary potassium restriction reduced measured plasma total calcium in the male mice. [murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339
Complete structured claim and evidence
The potassium-restricted male mice showed increased plasma parathyroid hormone.
Potassium → Plasma parathyroid hormone concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently.
endpoint
The potassium-restricted male mice showed increased plasma parathyroid hormone.
experimental-exposure
Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.
experimental_model
Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.
limitations
Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
The calcium-regulating hormone response accompanied altered calcium balance.
primary_references
[murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339
tissue_or_cell_type
kidney, blood and trabecular skeleton
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1316–1328
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. · source_derived_draft · unverified_draft
### mouse-k-restriction-pth The potassium-restricted male mice showed increased plasma parathyroid hormone. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The calcium-regulating hormone response accompanied altered calcium balance. organism: Mus musculus tissue_or_cell_type: kidney, blood and trabecular skeleton experimental_model: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. limitations: Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated. cross_nutrient: Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently. experimental-exposure: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. endpoint: The potassium-restricted male mice showed increased plasma parathyroid hormone. [murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339
Complete structured claim and evidence
Prolonged low-potassium feeding reduced trabecular bone mineral density in the male-mouse study.
Potassium → Trabecular bone mineral density source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently.
endpoint
Prolonged low-potassium feeding reduced trabecular bone mineral density in the male-mouse study.
experimental-exposure
Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.
experimental_model
Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model.
limitations
Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
The mineral imbalance extended to a measured skeletal endpoint.
primary_references
[murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339
tissue_or_cell_type
kidney, blood and trabecular skeleton
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1330–1342
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. · source_derived_draft · unverified_draft
### mouse-k-restriction-trabecular-bone Prolonged low-potassium feeding reduced trabecular bone mineral density in the male-mouse study. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mineral imbalance extended to a measured skeletal endpoint. organism: Mus musculus tissue_or_cell_type: kidney, blood and trabecular skeleton experimental_model: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. limitations: Male mouse model; co-occurring renal transporter and endocrine changes do not prove a complete causal chain or a human fracture effect. NCC-specific mediation is incompletely isolated. cross_nutrient: Dietary potassium restriction altered renal calcium balance, circulating PTH and trabecular mineral density; each endpoint is recorded independently. experimental-exposure: Male mice; two-week potassium-free discovery study and four/eight-week low-potassium study; urine/plasma minerals, renal proteomics, skeletal imaging, and constitutively active SPAK model. endpoint: Prolonged low-potassium feeding reduced trabecular bone mineral density in the male-mouse study. [murali-2026-calcium] Dietary potassium restriction causes hypercalciuria, hypocalcemia, and bone loss in male mice (2026). https://insight.jci.org/articles/view/196339 DOI: 10.1172/jci.insight.196339
Complete structured claim and evidence
Dietary potassium deficiency decreased proximal-tubule brush-border NaPi-IIc protein abundance in rats and mice.
Potassium → Sodium-phosphate cotransporter NaPi-IIc / SLC34A3 source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium deficiency changes sodium-phosphate transport machinery in an isoform-specific manner.
endpoint
Dietary potassium deficiency decreased proximal-tubule brush-border NaPi-IIc protein abundance in rats and mice.
experimental-exposure
Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses.
experimental_model
Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses.
limitations
Isoform abundance and localization do not apportion total phosphate flux; transporter-specific contributions and initiating signal remain unresolved.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus; Mus musculus where specified
plain_language
A sodium-phosphate uptake protein was depleted from the membrane.
primary_references
[breusegem-2009-phosphate] Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency (2009). https://pubmed.ncbi.nlm.nih.gov/19493963/ DOI: 10.1152/ajprenal.90765.2008
tissue_or_cell_type
renal proximal-tubule brush border
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1344–1356
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. · source_derived_draft · unverified_draft
### k-deficiency-napi2c-abundance Dietary potassium deficiency decreased proximal-tubule brush-border NaPi-IIc protein abundance in rats and mice. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sodium-phosphate uptake protein was depleted from the membrane. organism: Rattus norvegicus; Mus musculus where specified tissue_or_cell_type: renal proximal-tubule brush border experimental_model: Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. limitations: Isoform abundance and localization do not apportion total phosphate flux; transporter-specific contributions and initiating signal remain unresolved. cross_nutrient: Potassium deficiency changes sodium-phosphate transport machinery in an isoform-specific manner. experimental-exposure: Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. endpoint: Dietary potassium deficiency decreased proximal-tubule brush-border NaPi-IIc protein abundance in rats and mice. [breusegem-2009-phosphate] Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency (2009). https://pubmed.ncbi.nlm.nih.gov/19493963/ DOI: 10.1152/ajprenal.90765.2008
Complete structured claim and evidence
Dietary potassium deficiency decreased proximal-tubule brush-border PiT-2 abundance in rats and mice.
Potassium → PiT-2 / SLC20A2 source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium deficiency changes sodium-phosphate transport machinery in an isoform-specific manner.
endpoint
Dietary potassium deficiency decreased proximal-tubule brush-border PiT-2 abundance in rats and mice.
experimental-exposure
Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses.
experimental_model
Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses.
limitations
Isoform abundance and localization do not apportion total phosphate flux; transporter-specific contributions and initiating signal remain unresolved.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus; Mus musculus where specified
plain_language
A second, distinct sodium-phosphate transporter declined.
primary_references
[breusegem-2009-phosphate] Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency (2009). https://pubmed.ncbi.nlm.nih.gov/19493963/ DOI: 10.1152/ajprenal.90765.2008
tissue_or_cell_type
renal proximal-tubule brush border
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1358–1370
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. · source_derived_draft · unverified_draft
### k-deficiency-pit2-abundance Dietary potassium deficiency decreased proximal-tubule brush-border PiT-2 abundance in rats and mice. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second, distinct sodium-phosphate transporter declined. organism: Rattus norvegicus; Mus musculus where specified tissue_or_cell_type: renal proximal-tubule brush border experimental_model: Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. limitations: Isoform abundance and localization do not apportion total phosphate flux; transporter-specific contributions and initiating signal remain unresolved. cross_nutrient: Potassium deficiency changes sodium-phosphate transport machinery in an isoform-specific manner. experimental-exposure: Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. endpoint: Dietary potassium deficiency decreased proximal-tubule brush-border PiT-2 abundance in rats and mice. [breusegem-2009-phosphate] Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency (2009). https://pubmed.ncbi.nlm.nih.gov/19493963/ DOI: 10.1152/ajprenal.90765.2008
Complete structured claim and evidence
Potassium deficiency increased brush-border NaPi-IIa abundance in the studied rat experiments despite reduced total sodium-dependent phosphate transport.
Potassium → Sodium-phosphate cotransporter NaPi-IIa / SLC34A1 source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium deficiency changes sodium-phosphate transport machinery in an isoform-specific manner.
endpoint
Potassium deficiency increased brush-border NaPi-IIa abundance in the studied rat experiments despite reduced total sodium-dependent phosphate transport.
experimental-exposure
Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses.
experimental_model
Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses.
limitations
Isoform abundance and localization do not apportion total phosphate flux; transporter-specific contributions and initiating signal remain unresolved.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus; Mus musculus where specified
plain_language
More of one transporter did not mean greater overall phosphate recovery.
primary_references
[breusegem-2009-phosphate] Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency (2009). https://pubmed.ncbi.nlm.nih.gov/19493963/ DOI: 10.1152/ajprenal.90765.2008
tissue_or_cell_type
renal proximal-tubule brush border
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1372–1384
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. · source_derived_draft · unverified_draft
### k-deficiency-napi2a-abundance Potassium deficiency increased brush-border NaPi-IIa abundance in the studied rat experiments despite reduced total sodium-dependent phosphate transport. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: More of one transporter did not mean greater overall phosphate recovery. organism: Rattus norvegicus; Mus musculus where specified tissue_or_cell_type: renal proximal-tubule brush border experimental_model: Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. limitations: Isoform abundance and localization do not apportion total phosphate flux; transporter-specific contributions and initiating signal remain unresolved. cross_nutrient: Potassium deficiency changes sodium-phosphate transport machinery in an isoform-specific manner. experimental-exposure: Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. endpoint: Potassium deficiency increased brush-border NaPi-IIa abundance in the studied rat experiments despite reduced total sodium-dependent phosphate transport. [breusegem-2009-phosphate] Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency (2009). https://pubmed.ncbi.nlm.nih.gov/19493963/ DOI: 10.1152/ajprenal.90765.2008
Complete structured claim and evidence
Eleven days of potassium deprivation reduced AQP2 abundance in rat cortical and medullary collecting ducts.
Potassium → Aquaporin-2 / AQP2 source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
endpoint
Eleven days of potassium deprivation reduced AQP2 abundance in rat cortical and medullary collecting ducts.
experimental-exposure
Rats with 11 days of potassium deprivation; AQP2 immunoblot/immunocytochemistry, urine volume, and potassium refeeding.
experimental_model
Rats with 11 days of potassium deprivation; AQP2 immunoblot/immunocytochemistry, urine volume, and potassium refeeding.
limitations
Parallel changes and refeeding support reversibility, but no AQP2-specific rescue isolated its complete contribution.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
Less water-channel protein accompanied the concentrating defect.
primary_references
[marples-1996-aqp2] Hypokalemia-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla and cortex (1996). https://pubmed.ncbi.nlm.nih.gov/8621781/ DOI: 10.1172/JCI118628
tissue_or_cell_type
cortical and inner medullary collecting ducts
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1386–1397
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats with 11 days of potassium deprivation; AQP2 immunoblot/immunocytochemistry, urine volume, and potassium refeeding. · source_derived_draft · unverified_draft
### k-depletion-aqp2-abundance Eleven days of potassium deprivation reduced AQP2 abundance in rat cortical and medullary collecting ducts. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less water-channel protein accompanied the concentrating defect. organism: Rattus norvegicus tissue_or_cell_type: cortical and inner medullary collecting ducts experimental_model: Rats with 11 days of potassium deprivation; AQP2 immunoblot/immunocytochemistry, urine volume, and potassium refeeding. limitations: Parallel changes and refeeding support reversibility, but no AQP2-specific rescue isolated its complete contribution. experimental-exposure: Rats with 11 days of potassium deprivation; AQP2 immunoblot/immunocytochemistry, urine volume, and potassium refeeding. endpoint: Eleven days of potassium deprivation reduced AQP2 abundance in rat cortical and medullary collecting ducts. [marples-1996-aqp2] Hypokalemia-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla and cortex (1996). https://pubmed.ncbi.nlm.nih.gov/8621781/ DOI: 10.1172/JCI118628
Complete structured claim and evidence
After one day of potassium deprivation, AQP2 localized in autophagic compartments in rat inner medullary collecting-duct cells.
Potassium → AQP2 localization in autophagic compartments source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
endpoint
After one day of potassium deprivation, AQP2 localized in autophagic compartments in rat inner medullary collecting-duct cells.
experimental-exposure
Rats fed potassium-free diet for one day; IMCD proteomics, immunoblotting, immunogold electron microscopy, and refeeding.
experimental_model
Rats fed potassium-free diet for one day; IMCD proteomics, immunoblotting, immunogold electron microscopy, and refeeding.
limitations
Autophagy inhibition was not performed; colocalization and recovery do not establish that autophagic AQP2 degradation alone caused polyuria.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
Water-channel disposal began early, alongside AQP2 loss.
primary_references
[khositseth-2015-aqp2] Autophagic degradation of aquaporin-2 is an early event in hypokalemia-induced nephrogenic diabetes insipidus (2015). https://www.nature.com/articles/srep18311 DOI: 10.1038/srep18311
tissue_or_cell_type
inner medullary collecting duct
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1399–1410
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats fed potassium-free diet for one day; IMCD proteomics, immunoblotting, immunogold electron microscopy, and refeeding. · source_derived_draft · unverified_draft
### early-k-deprivation-aqp2-autophagic-localization After one day of potassium deprivation, AQP2 localized in autophagic compartments in rat inner medullary collecting-duct cells. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Water-channel disposal began early, alongside AQP2 loss. organism: Rattus norvegicus tissue_or_cell_type: inner medullary collecting duct experimental_model: Rats fed potassium-free diet for one day; IMCD proteomics, immunoblotting, immunogold electron microscopy, and refeeding. limitations: Autophagy inhibition was not performed; colocalization and recovery do not establish that autophagic AQP2 degradation alone caused polyuria. experimental-exposure: Rats fed potassium-free diet for one day; IMCD proteomics, immunoblotting, immunogold electron microscopy, and refeeding. endpoint: After one day of potassium deprivation, AQP2 localized in autophagic compartments in rat inner medullary collecting-duct cells. [khositseth-2015-aqp2] Autophagic degradation of aquaporin-2 is an early event in hypokalemia-induced nephrogenic diabetes insipidus (2015). https://www.nature.com/articles/srep18311 DOI: 10.1038/srep18311
Complete structured claim and evidence
Dietary potassium restriction reduced Ser256-phosphorylated AQP2 in cortical and medullary collecting ducts of both male and female mice.
Potassium → Ser256-phosphorylated AQP2 source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
endpoint
Dietary potassium restriction reduced Ser256-phosphorylated AQP2 in cortical and medullary collecting ducts of both male and female mice.
experimental-exposure
Male and female C57BL/6J mice exposed to graded potassium restriction for eight days; water-balance and collecting-duct signaling measurements.
experimental_model
Male and female C57BL/6J mice exposed to graded potassium restriction for eight days; water-balance and collecting-duct signaling measurements.
limitations
Sex and segment influenced severity; this does not establish a universal human plasma-potassium threshold or a unique responsible kinase.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
The channel activation/trafficking state changed even where total protein loss was less marked.
primary_references
[al-qusairi-2021-vasopressin] Rapid development of vasopressin resistance in dietary K+ deficiency (2021). https://pubmed.ncbi.nlm.nih.gov/33749322/ DOI: 10.1152/ajprenal.00655.2020
tissue_or_cell_type
cortical and medullary collecting duct
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1412–1423
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Male and female C57BL/6J mice exposed to graded potassium restriction for eight days; water-balance and collecting-duct signaling measurements. · source_derived_draft · unverified_draft
### k-restriction-lowers-aqp2-ser256 Dietary potassium restriction reduced Ser256-phosphorylated AQP2 in cortical and medullary collecting ducts of both male and female mice. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The channel activation/trafficking state changed even where total protein loss was less marked. organism: Mus musculus tissue_or_cell_type: cortical and medullary collecting duct experimental_model: Male and female C57BL/6J mice exposed to graded potassium restriction for eight days; water-balance and collecting-duct signaling measurements. limitations: Sex and segment influenced severity; this does not establish a universal human plasma-potassium threshold or a unique responsible kinase. experimental-exposure: Male and female C57BL/6J mice exposed to graded potassium restriction for eight days; water-balance and collecting-duct signaling measurements. endpoint: Dietary potassium restriction reduced Ser256-phosphorylated AQP2 in cortical and medullary collecting ducts of both male and female mice. [al-qusairi-2021-vasopressin] Rapid development of vasopressin resistance in dietary K+ deficiency (2021). https://pubmed.ncbi.nlm.nih.gov/33749322/ DOI: 10.1152/ajprenal.00655.2020
Complete structured claim and evidence
Principal-cell Atg7 deletion worsened urine-concentrating impairment during potassium depletion rather than rescuing it.
Principal-cell Atg7 deletion → Renal urine concentrating capacity source_derived_draftungraded
Experimental context and source evidence
availability_state
machinery_impairment Imported condition classification; unverified.
endpoint
Principal-cell Atg7 deletion worsened urine-concentrating impairment during potassium depletion rather than rescuing it.
experimental-exposure
Principal-cell Atg7 conditional knockout and floxed control mice on normal or potassium-free diet for two weeks.
experimental_model
Principal-cell Atg7 conditional knockout and floxed control mice on normal or potassium-free diet for two weeks.
limitations
Knockout already altered basal urine concentration and caused compensatory degradation changes; this is not evidence against every role for autophagy.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
Blocking one protein-disposal pathway did not restore water balance; channel phosphorylation and localization still mattered.
primary_references
[kim-2019-atg7-aqp2] Atg7-dependent canonical autophagy regulates the degradation of aquaporin 2 in prolonged hypokalemia (2019). https://www.nature.com/articles/s41598-019-39702-4 DOI: 10.1038/s41598-019-39702-4
tissue_or_cell_type
collecting-duct principal cells
trigger_kind
machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1425–1436
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Principal-cell Atg7 conditional knockout and floxed control mice on normal or potassium-free diet for two weeks. · source_derived_draft · unverified_draft
### atg7-loss-worsens-hypokalemic-concentrating-defect Principal-cell Atg7 deletion worsened urine-concentrating impairment during potassium depletion rather than rescuing it. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking one protein-disposal pathway did not restore water balance; channel phosphorylation and localization still mattered. organism: Mus musculus tissue_or_cell_type: collecting-duct principal cells experimental_model: Principal-cell Atg7 conditional knockout and floxed control mice on normal or potassium-free diet for two weeks. limitations: Knockout already altered basal urine concentration and caused compensatory degradation changes; this is not evidence against every role for autophagy. experimental-exposure: Principal-cell Atg7 conditional knockout and floxed control mice on normal or potassium-free diet for two weeks. endpoint: Principal-cell Atg7 deletion worsened urine-concentrating impairment during potassium depletion rather than rescuing it. [kim-2019-atg7-aqp2] Atg7-dependent canonical autophagy regulates the degradation of aquaporin 2 in prolonged hypokalemia (2019). https://www.nature.com/articles/s41598-019-39702-4 DOI: 10.1038/s41598-019-39702-4
Complete structured claim and evidence
Potassium citrate reduced new stone formation relative to placebo among participants followed for three years in the hypocitraturic calcium-stone trial.
Potassium citrate → Calcium stone formation rate source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Citrate/alkali coadministration with potassium modifies calcium-stone formation in hypocitraturic stone formers.
endpoint
Potassium citrate reduced new stone formation relative to placebo among participants followed for three years in the hypocitraturic calcium-stone trial.
experimental-exposure
Fifty-seven people with recurrent calcium stones and hypocitraturia randomized to potassium citrate 30-60 mEq/day or placebo; three-year outcomes in 18 and 20 respectively.
experimental_model
Fifty-seven people with recurrent calcium stones and hypocitraturia randomized to potassium citrate 30-60 mEq/day or placebo; three-year outcomes in 18 and 20 respectively.
limitations
57 randomized but 38 contributed the cited three-year comparison; potassium, citrate and alkalinization were cointerventions. Not a potassium-cation-only effect or treatment recommendation.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
The combined salt changed a stone outcome in a selected clinical group.
primary_references
[barcelo-1993-stones] Randomized double-blind study of potassium citrate in idiopathic hypocitraturic calcium nephrolithiasis (1993). https://www.sciencedirect.com/science/article/pii/S0022534717358883 DOI: 10.1016/S0022-5347(17)35888-3
tissue_or_cell_type
urinary tract
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1438–1450
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fifty-seven people with recurrent calcium stones and hypocitraturia randomized to potassium citrate 30-60 mEq/day or placebo; three-year outcomes in 18 and 20 respectively. · source_derived_draft · unverified_draft
### potassium-citrate-reduces-calcium-stone-formation Potassium citrate reduced new stone formation relative to placebo among participants followed for three years in the hypocitraturic calcium-stone trial. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The combined salt changed a stone outcome in a selected clinical group. organism: Homo sapiens tissue_or_cell_type: urinary tract experimental_model: Fifty-seven people with recurrent calcium stones and hypocitraturia randomized to potassium citrate 30-60 mEq/day or placebo; three-year outcomes in 18 and 20 respectively. limitations: 57 randomized but 38 contributed the cited three-year comparison; potassium, citrate and alkalinization were cointerventions. Not a potassium-cation-only effect or treatment recommendation. cross_nutrient: Citrate/alkali coadministration with potassium modifies calcium-stone formation in hypocitraturic stone formers. experimental-exposure: Fifty-seven people with recurrent calcium stones and hypocitraturia randomized to potassium citrate 30-60 mEq/day or placebo; three-year outcomes in 18 and 20 respectively. endpoint: Potassium citrate reduced new stone formation relative to placebo among participants followed for three years in the hypocitraturic calcium-stone trial. [barcelo-1993-stones] Randomized double-blind study of potassium citrate in idiopathic hypocitraturic calcium nephrolithiasis (1993). https://www.sciencedirect.com/science/article/pii/S0022534717358883 DOI: 10.1016/S0022-5347(17)35888-3
Complete structured claim and evidence
Modeled potassium absorption was high and not detectably different between potatoes and gluconate in the short feeding comparison.
Potassium → Intestinal potassium absorption source_derived_draftungraded
Experimental context and source evidence
experimental_model
Five-day feeding periods.
exposure
Added 20, 40 or 60 mEq/day; fries evaluated separately.
limitations
Specific foods and healthy participants; does not rank all foods or establish long-term outcomes.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
Potassium in the tested food and salt both reached the body.
primary_references
[k-macdonald2016] Bioavailability of potassium from potatoes and potassium gluconate: a randomized dose response trial (2016). https://pubmed.ncbi.nlm.nih.gov/27413123/ DOI: 10.3945/ajcn.115.127225
tissue_or_cell_type
Gastrointestinal tract; modeled balance
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1452–1462
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Five-day feeding periods. · source_derived_draft · unverified_draft
### k-potato-gluconate-absorption Modeled potassium absorption was high and not detectably different between potatoes and gluconate in the short feeding comparison. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium in the tested food and salt both reached the body. organism: Homo sapiens tissue_or_cell_type: Gastrointestinal tract; modeled balance experimental_model: Five-day feeding periods. limitations: Specific foods and healthy participants; does not rank all foods or establish long-term outcomes. exposure: Added 20, 40 or 60 mEq/day; fries evaluated separately. [k-macdonald2016] Bioavailability of potassium from potatoes and potassium gluconate: a randomized dose response trial (2016). https://pubmed.ncbi.nlm.nih.gov/27413123/ DOI: 10.3945/ajcn.115.127225
Complete structured claim and evidence
Urinary potassium recovery was greater after potato intake than after the supplement despite no detected source difference in serum exposure.
Potassium gluconate → Urinary potassium excretion source_derived_draftungraded
Experimental context and source evidence
experimental_model
Same feeding study.
limitations
Urinary potassium alone is not an exact measure of food intake or intracellular stores.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
Urinary recovery and absorption are related but distinct measurements.
primary_references
[k-macdonald2016] Bioavailability of potassium from potatoes and potassium gluconate: a randomized dose response trial (2016). https://pubmed.ncbi.nlm.nih.gov/27413123/ DOI: 10.3945/ajcn.115.127225
tissue_or_cell_type
Urine and serum
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1464–1473
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Same feeding study. · source_derived_draft · unverified_draft
### k-potato-urinary-recovery Urinary potassium recovery was greater after potato intake than after the supplement despite no detected source difference in serum exposure. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Urinary recovery and absorption are related but distinct measurements. organism: Homo sapiens tissue_or_cell_type: Urine and serum experimental_model: Same feeding study. limitations: Urinary potassium alone is not an exact measure of food intake or intracellular stores. [k-macdonald2016] Bioavailability of potassium from potatoes and potassium gluconate: a randomized dose response trial (2016). https://pubmed.ncbi.nlm.nih.gov/27413123/ DOI: 10.3945/ajcn.115.127225
Complete structured claim and evidence
Patients with end-stage renal disease showed higher colonic BK expression and approximately threefold higher rectal potassium secretion than controls.
Large-conductance calcium-activated potassium channel alpha subunit → Colonic potassium secretion source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Kidney failure -> extra-renal potassium handling.
experimental_model
Small human biopsy and rectal-dialysis groups.
limitations
Expression plus association does not identify every flux pathway; no diet intervention.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
The colon can increase its potassium-disposal role when kidney function is severely reduced.
primary_references
[k-sandle2005] Enhanced large intestinal potassium permeability in end-stage renal disease (2005). https://pubmed.ncbi.nlm.nih.gov/15772943/ DOI: 10.1002/path.1750
tissue_or_cell_type
Human distal colon and rectum
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1475–1485
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Small human biopsy and rectal-dialysis groups. · source_derived_draft · unverified_draft
### k-esrd-colonic-bk-upregulation Patients with end-stage renal disease showed higher colonic BK expression and approximately threefold higher rectal potassium secretion than controls. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The colon can increase its potassium-disposal role when kidney function is severely reduced. organism: Homo sapiens tissue_or_cell_type: Human distal colon and rectum experimental_model: Small human biopsy and rectal-dialysis groups. limitations: Expression plus association does not identify every flux pathway; no diet intervention. cross_nutrient: Kidney failure -> extra-renal potassium handling. [k-sandle2005] Enhanced large intestinal potassium permeability in end-stage renal disease (2005). https://pubmed.ncbi.nlm.nih.gov/15772943/ DOI: 10.1002/path.1750
Complete structured claim and evidence
Luminal barium reduced potassium secretion by about 45% in the kidney-failure group, supporting a potassium-channel contribution.
Barium ion → Colonic potassium secretion source_derived_draftungraded
Experimental context and source evidence
experimental_model
Rectal dialysis with 5 mmol/L barium.
limitations
Barium is not BK-specific; combine this with expression evidence without asserting exclusive BK mediation.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
Part of the extra gut potassium loss depended on a blocker-sensitive pathway.
primary_references
[k-sandle2005] Enhanced large intestinal potassium permeability in end-stage renal disease (2005). https://pubmed.ncbi.nlm.nih.gov/15772943/ DOI: 10.1002/path.1750
tissue_or_cell_type
Human rectum
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1487–1496
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rectal dialysis with 5 mmol/L barium. · source_derived_draft · unverified_draft
### k-esrd-colonic-barium-sensitive-secretion Luminal barium reduced potassium secretion by about 45% in the kidney-failure group, supporting a potassium-channel contribution. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Part of the extra gut potassium loss depended on a blocker-sensitive pathway. organism: Homo sapiens tissue_or_cell_type: Human rectum experimental_model: Rectal dialysis with 5 mmol/L barium. limitations: Barium is not BK-specific; combine this with expression evidence without asserting exclusive BK mediation. [k-sandle2005] Enhanced large intestinal potassium permeability in end-stage renal disease (2005). https://pubmed.ncbi.nlm.nih.gov/15772943/ DOI: 10.1002/path.1750
Complete structured claim and evidence
Marked BK overexpression accompanied colonic potassium-secretory diarrhea and hypokalemia in the reported patient.
Colonic BK channel abundance → Colonic potassium secretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
experimental_model
Single case; symptoms resolved after colectomy.
limitations
The proposed shock/ischemia-to-BK chain remains a hypothesis.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
Severe potassium loss can occur through the gut even in kidney failure.
primary_references
[k-van-dinter2008] Over-expression of colonic K+ channels associated with severe potassium secretory diarrhoea after haemorrhagic shock (2008). https://pubmed.ncbi.nlm.nih.gov/18653901/ DOI: 10.1093/ndt/gfn411
tissue_or_cell_type
Human colon
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1498–1507
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single case; symptoms resolved after colectomy. · source_derived_draft · unverified_draft
### k-secretory-diarrhea-bk-case Marked BK overexpression accompanied colonic potassium-secretory diarrhea and hypokalemia in the reported patient. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Severe potassium loss can occur through the gut even in kidney failure. organism: Homo sapiens tissue_or_cell_type: Human colon experimental_model: Single case; symptoms resolved after colectomy. limitations: The proposed shock/ischemia-to-BK chain remains a hypothesis. [k-van-dinter2008] Over-expression of colonic K+ channels associated with severe potassium secretory diarrhoea after haemorrhagic shock (2008). https://pubmed.ncbi.nlm.nih.gov/18653901/ DOI: 10.1093/ndt/gfn411
Complete structured claim and evidence
At fixed sodium intake, potassium depletion reduced urinary sodium from 110 to 83 mmol/day in this crossover.
Potassium → Urinary sodium excretion source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium -> sodium balance.
experimental_model
12 hypertensive adults; ten-day periods.
exposure
16 versus 96 mmol/day K; sodium 120 mmol/day.
limitations
Supports retention physiology; the human study did not measure the Kir4.1-WNK-NCC chain.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
A potassium shortage changed how the kidney handled sodium.
primary_references
[k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77
tissue_or_cell_type
Kidney and urine
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1509–1520
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 12 hypertensive adults; ten-day periods. · source_derived_draft · unverified_draft
### k-depletion-human-sodium-retention At fixed sodium intake, potassium depletion reduced urinary sodium from 110 to 83 mmol/day in this crossover. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A potassium shortage changed how the kidney handled sodium. organism: Homo sapiens tissue_or_cell_type: Kidney and urine experimental_model: 12 hypertensive adults; ten-day periods. limitations: Supports retention physiology; the human study did not measure the Kir4.1-WNK-NCC chain. cross_nutrient: Potassium -> sodium balance. exposure: 16 versus 96 mmol/day K; sodium 120 mmol/day. [k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77
Complete structured claim and evidence
Low potassium increased systolic/diastolic pressure by about 7/6 mmHg in the same crossover.
Potassium → Arterial blood pressure source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium/sodium balance -> pressure.
experimental_model
Same cohort and intervention.
limitations
Not an independent replication or proof of one molecular mediator.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
In this setting, lowering potassium raised blood pressure.
primary_references
[k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77
tissue_or_cell_type
Systemic circulation
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1522–1532
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Same cohort and intervention. · source_derived_draft · unverified_draft
### k-depletion-human-pressure Low potassium increased systolic/diastolic pressure by about 7/6 mmHg in the same crossover. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this setting, lowering potassium raised blood pressure. organism: Homo sapiens tissue_or_cell_type: Systemic circulation experimental_model: Same cohort and intervention. limitations: Not an independent replication or proof of one molecular mediator. cross_nutrient: Potassium/sodium balance -> pressure. [k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77
Complete structured claim and evidence
The depletion period also increased urinary calcium and phosphate and plasma immunoreactive PTH.
Potassium → Plasma parathyroid hormone concentration source_derived_draftungraded
Experimental context and source evidence
availability_state
nutrient_deficiency Imported condition classification; unverified.
cross_nutrient
Potassium -> calcium/phosphate/PTH observations.
experimental_model
Concurrent mineral and hormone measurements.
limitations
Co-occurrence does not establish that PTH caused every excretion change.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
Potassium depletion affected calcium-phosphate regulation alongside sodium handling.
primary_references
[k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77
tissue_or_cell_type
Plasma and urine
trigger_kind
nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1534–1544
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Concurrent mineral and hormone measurements. · source_derived_draft · unverified_draft
### k-depletion-human-mineral-pth-response The depletion period also increased urinary calcium and phosphate and plasma immunoreactive PTH. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium depletion affected calcium-phosphate regulation alongside sodium handling. organism: Homo sapiens tissue_or_cell_type: Plasma and urine experimental_model: Concurrent mineral and hormone measurements. limitations: Co-occurrence does not establish that PTH caused every excretion change. cross_nutrient: Potassium -> calcium/phosphate/PTH observations. [k-krishna1991] Potassium depletion exacerbates essential hypertension (1991). https://pubmed.ncbi.nlm.nih.gov/2058867/ DOI: 10.7326/0003-4819-115-2-77
Complete structured claim and evidence
Potassium supplementation reduced 24-hour pressure by approximately 3.9/1.6 mmHg under controlled feeding.
Potassium → Arterial blood pressure source_derived_draftungraded
Experimental context and source evidence
experimental_model
Four-week crossover; 36 completers.
limitations
Untreated elevated-pressure adults with relatively low baseline sodium/potassium intake; no detected pulse-wave-velocity benefit.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
The blood-pressure effect was measured directly in this trial.
primary_references
[k-gijsbers2015-bp] Effects of sodium and potassium supplementation on blood pressure and arterial stiffness: a fully controlled dietary intervention study (2015). https://pubmed.ncbi.nlm.nih.gov/25673113/ DOI: 10.1038/jhh.2015.3
tissue_or_cell_type
Systemic circulation
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1546–1555
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-week crossover; 36 completers. · source_derived_draft · unverified_draft
### k-controlled-feeding-pressure Potassium supplementation reduced 24-hour pressure by approximately 3.9/1.6 mmHg under controlled feeding. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The blood-pressure effect was measured directly in this trial. organism: Homo sapiens tissue_or_cell_type: Systemic circulation experimental_model: Four-week crossover; 36 completers. limitations: Untreated elevated-pressure adults with relatively low baseline sodium/potassium intake; no detected pulse-wave-velocity benefit. [k-gijsbers2015-bp] Effects of sodium and potassium supplementation on blood pressure and arterial stiffness: a fully controlled dietary intervention study (2015). https://pubmed.ncbi.nlm.nih.gov/25673113/ DOI: 10.1038/jhh.2015.3
Complete structured claim and evidence
The endothelial substudy found a 1.16-percentage-point increase in flow-mediated dilation with potassium.
Potassium → Brachial artery flow-mediated dilation source_derived_draftungraded
Experimental context and source evidence
experimental_model
FMD subgroup, 22-24 usable measurements per comparison.
limitations
Same parent trial; no direct demonstration of nitric oxide or a particular channel as mediator.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
A vessel-response measurement improved in this subgroup.
primary_references
[k-gijsbers2015-fmd] Effects of sodium and potassium supplementation on endothelial function: a fully controlled dietary intervention study (2015). https://pubmed.ncbi.nlm.nih.gov/26343780/ DOI: 10.1017/s0007114515002986
tissue_or_cell_type
Brachial artery
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1557–1566
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · FMD subgroup, 22-24 usable measurements per comparison. · source_derived_draft · unverified_draft
### k-controlled-feeding-fmd The endothelial substudy found a 1.16-percentage-point increase in flow-mediated dilation with potassium. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A vessel-response measurement improved in this subgroup. organism: Homo sapiens tissue_or_cell_type: Brachial artery experimental_model: FMD subgroup, 22-24 usable measurements per comparison. limitations: Same parent trial; no direct demonstration of nitric oxide or a particular channel as mediator. [k-gijsbers2015-fmd] Effects of sodium and potassium supplementation on endothelial function: a fully controlled dietary intervention study (2015). https://pubmed.ncbi.nlm.nih.gov/26343780/ DOI: 10.1017/s0007114515002986
Complete structured claim and evidence
Potassium increased aldosterone, renin and copeptin in the post-hoc hormone analysis while blood pressure fell.
Potassium → Plasma aldosterone concentration source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Potassium -> endocrine regulation; sodium/volume context retained.
experimental_model
35 participants from the same feeding trial.
limitations
Post-hoc circulating markers do not identify receptor signaling or a universal endocrine response.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
A hormone response can accompany a pressure reduction rather than imply the opposite outcome.
primary_references
[k-gijsbers2016-hormones] Effects of potassium supplementation on markers of osmoregulation and volume regulation: results of a fully controlled dietary intervention study (2016). https://pubmed.ncbi.nlm.nih.gov/26599222/ DOI: 10.1097/hjh.0000000000000786
tissue_or_cell_type
Plasma
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1568–1578
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 35 participants from the same feeding trial. · source_derived_draft · unverified_draft
### k-controlled-feeding-regulatory-hormones Potassium increased aldosterone, renin and copeptin in the post-hoc hormone analysis while blood pressure fell. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A hormone response can accompany a pressure reduction rather than imply the opposite outcome. organism: Homo sapiens tissue_or_cell_type: Plasma experimental_model: 35 participants from the same feeding trial. limitations: Post-hoc circulating markers do not identify receptor signaling or a universal endocrine response. cross_nutrient: Potassium -> endocrine regulation; sodium/volume context retained. [k-gijsbers2016-hormones] Effects of potassium supplementation on markers of osmoregulation and volume regulation: results of a fully controlled dietary intervention study (2016). https://pubmed.ncbi.nlm.nih.gov/26599222/ DOI: 10.1097/hjh.0000000000000786
Complete structured claim and evidence
Acetylcholine produced a local potassium rise and hyperpolarization sensitive to combined calcium-activated potassium-channel blockers in rat arteries.
Vascular calcium-activated potassium channels → Potassium ion source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Calcium-regulated channel activity -> local potassium signal.
experimental_model
Rat isolated arteries; potassium electrodes and blockers.
limitations
Pharmacology does not uniquely identify an SK/IK gene; not a dietary intervention.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
Potassium can act locally as a signal between vessel cells.
primary_references
[k-edwards1998] K+ is an endothelium-derived hyperpolarizing factor in rat arteries (1998). https://pubmed.ncbi.nlm.nih.gov/9834033/ DOI: 10.1038/24388
tissue_or_cell_type
Arterial endothelium and myoendothelial space
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1580–1590
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat isolated arteries; potassium electrodes and blockers. · source_derived_draft · unverified_draft
### k-vascular-endothelial-release Acetylcholine produced a local potassium rise and hyperpolarization sensitive to combined calcium-activated potassium-channel blockers in rat arteries. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium can act locally as a signal between vessel cells. organism: Rattus norvegicus tissue_or_cell_type: Arterial endothelium and myoendothelial space experimental_model: Rat isolated arteries; potassium electrodes and blockers. limitations: Pharmacology does not uniquely identify an SK/IK gene; not a dietary intervention. cross_nutrient: Calcium-regulated channel activity -> local potassium signal. [k-edwards1998] K+ is an endothelium-derived hyperpolarizing factor in rat arteries (1998). https://pubmed.ncbi.nlm.nih.gov/9834033/ DOI: 10.1038/24388
Complete structured claim and evidence
Small extracellular potassium elevations relaxed the studied rat arteries through ouabain/barium-sensitive pump and inward-rectifier pathways.
Potassium ion → Vascular smooth muscle hyperpolarization source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Potassium/sodium pump and potassium channels -> vessel response.
experimental_model
Isolated rat artery electrophysiology.
limitations
Channel family inference; not every artery or potassium concentration responds this way.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
A modest local potassium rise can relax a vessel under particular conditions.
primary_references
[k-edwards1998] K+ is an endothelium-derived hyperpolarizing factor in rat arteries (1998). https://pubmed.ncbi.nlm.nih.gov/9834033/ DOI: 10.1038/24388
tissue_or_cell_type
Arterial smooth muscle
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1592–1602
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated rat artery electrophysiology. · source_derived_draft · unverified_draft
### k-vascular-pump-kir-relaxation Small extracellular potassium elevations relaxed the studied rat arteries through ouabain/barium-sensitive pump and inward-rectifier pathways. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A modest local potassium rise can relax a vessel under particular conditions. organism: Rattus norvegicus tissue_or_cell_type: Arterial smooth muscle experimental_model: Isolated rat artery electrophysiology. limitations: Channel family inference; not every artery or potassium concentration responds this way. cross_nutrient: Potassium/sodium pump and potassium channels -> vessel response. [k-edwards1998] K+ is an endothelium-derived hyperpolarizing factor in rat arteries (1998). https://pubmed.ncbi.nlm.nih.gov/9834033/ DOI: 10.1038/24388
Complete structured claim and evidence
Local potassium stimulated Kir2.1-dependent capillary signaling; endothelial Kir2.1 deletion abolished the tested potassium-evoked upstream dilation.
Potassium ion → KCNJ2 / Kir2.1 source_derived_draftungraded
Experimental context and source evidence
experimental_model
Mouse isolated capillary-arteriole preparations and in-vivo imaging.
exposure
Local 10 mmol/L K application.
limitations
Local experimental potassium exposure, not dietary supplementation.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
Brain capillaries can send an electrical signal upstream to their supplying arteriole.
primary_references
[k-longden2017] Capillary K+-sensing initiates retrograde hyperpolarization to increase local cerebral blood flow (2017). https://pubmed.ncbi.nlm.nih.gov/28319610/ DOI: 10.1038/nn.4533
tissue_or_cell_type
Brain capillary endothelium and upstream arterioles
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1604–1614
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse isolated capillary-arteriole preparations and in-vivo imaging. · source_derived_draft · unverified_draft
### k-capillary-kir21-sensing Local potassium stimulated Kir2.1-dependent capillary signaling; endothelial Kir2.1 deletion abolished the tested potassium-evoked upstream dilation. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Brain capillaries can send an electrical signal upstream to their supplying arteriole. organism: Mus musculus tissue_or_cell_type: Brain capillary endothelium and upstream arterioles experimental_model: Mouse isolated capillary-arteriole preparations and in-vivo imaging. limitations: Local experimental potassium exposure, not dietary supplementation. exposure: Local 10 mmol/L K application. [k-longden2017] Capillary K+-sensing initiates retrograde hyperpolarization to increase local cerebral blood flow (2017). https://pubmed.ncbi.nlm.nih.gov/28319610/ DOI: 10.1038/nn.4533
Complete structured claim and evidence
Endothelial Kir2.1 deletion reduced whisker-stimulation cerebral blood-flow responses by roughly half.
KCNJ2 / Kir2.1 → Cerebral functional hyperemia source_derived_draftungraded
Experimental context and source evidence
experimental_model
Mouse endothelial knockout and cortical flow measurement.
limitations
Residual responses require other contributors; no cognitive or dietary outcome tested.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Mus musculus
plain_language
This potassium-sensing pathway contributed to activity-linked blood supply but did not account for all of it.
primary_references
[k-longden2017] Capillary K+-sensing initiates retrograde hyperpolarization to increase local cerebral blood flow (2017). https://pubmed.ncbi.nlm.nih.gov/28319610/ DOI: 10.1038/nn.4533
tissue_or_cell_type
Cerebral microcirculation
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1616–1625
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse endothelial knockout and cortical flow measurement. · source_derived_draft · unverified_draft
### k-kir21-functional-hyperemia Endothelial Kir2.1 deletion reduced whisker-stimulation cerebral blood-flow responses by roughly half. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: This potassium-sensing pathway contributed to activity-linked blood supply but did not account for all of it. organism: Mus musculus tissue_or_cell_type: Cerebral microcirculation experimental_model: Mouse endothelial knockout and cortical flow measurement. limitations: Residual responses require other contributors; no cognitive or dietary outcome tested. [k-longden2017] Capillary K+-sensing initiates retrograde hyperpolarization to increase local cerebral blood flow (2017). https://pubmed.ncbi.nlm.nih.gov/28319610/ DOI: 10.1038/nn.4533
Complete structured claim and evidence
In pressurized rat mesenteric arteries, raised potassium did not reliably reproduce acetylcholine-evoked EDHF relaxation or hyperpolarization.
Potassium ion → Arteriolar dilation source_derived_draftungraded
Experimental context and source evidence
experimental_model
Myogenic tone at 60/90 mmHg, nitric oxide and prostanoid pathways blocked.
limitations
Preparation and tone differ from earlier work; record scope rather than inventing an unexplained contradiction.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Rattus norvegicus
plain_language
Potassium is not a universal explanation for endothelial relaxation.
primary_references
[k-brochet2014] A comparison of responses to raised extracellular potassium and endothelium-derived hyperpolarizing factor (EDHF) in rat pressurised mesenteric arteries (2014). https://pubmed.ncbi.nlm.nih.gov/25372386/ DOI: 10.1371/journal.pone.0111977
tissue_or_cell_type
Mesenteric resistance arteries
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1627–1636
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Myogenic tone at 60/90 mmHg, nitric oxide and prostanoid pathways blocked. · source_derived_draft · unverified_draft
### k-vascular-edhf-context-boundary In pressurized rat mesenteric arteries, raised potassium did not reliably reproduce acetylcholine-evoked EDHF relaxation or hyperpolarization. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium is not a universal explanation for endothelial relaxation. organism: Rattus norvegicus tissue_or_cell_type: Mesenteric resistance arteries experimental_model: Myogenic tone at 60/90 mmHg, nitric oxide and prostanoid pathways blocked. limitations: Preparation and tone differ from earlier work; record scope rather than inventing an unexplained contradiction. [k-brochet2014] A comparison of responses to raised extracellular potassium and endothelium-derived hyperpolarizing factor (EDHF) in rat pressurised mesenteric arteries (2014). https://pubmed.ncbi.nlm.nih.gov/25372386/ DOI: 10.1371/journal.pone.0111977
Complete structured claim and evidence
Two weeks of KCl raised mean plasma potassium from 4.3 to 4.7 mmol/L; 21 of 191 CKD participants developed hyperkalemia.
Potassium chloride → Plasma potassium concentration source_derived_draftungraded
Experimental context and source evidence
experimental_model
Uncontrolled run-in; CKD G3b-4.
exposure
40 mmol/day KCl; 83% used RAAS inhibitors.
limitations
11% is this cohort rate, not general-population risk or a dose recommendation.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
Reduced kidney clearance changes the response to an added potassium load.
primary_references
[k-gritter2022] Effects of Short-Term Potassium Chloride Supplementation in Patients with CKD (2022). https://pubmed.ncbi.nlm.nih.gov/35609996/ DOI: 10.1681/asn.2022020147
tissue_or_cell_type
Plasma
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1638–1648
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Uncontrolled run-in; CKD G3b-4. · source_derived_draft · unverified_draft
### k-ckd-kcl-plasma-rise Two weeks of KCl raised mean plasma potassium from 4.3 to 4.7 mmol/L; 21 of 191 CKD participants developed hyperkalemia. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reduced kidney clearance changes the response to an added potassium load. organism: Homo sapiens tissue_or_cell_type: Plasma experimental_model: Uncontrolled run-in; CKD G3b-4. limitations: 11% is this cohort rate, not general-population risk or a dose recommendation. exposure: 40 mmol/day KCl; 83% used RAAS inhibitors. [k-gritter2022] Effects of Short-Term Potassium Chloride Supplementation in Patients with CKD (2022). https://pubmed.ncbi.nlm.nih.gov/35609996/ DOI: 10.1681/asn.2022020147
Complete structured claim and evidence
The same KCl run-in modestly lowered mean bicarbonate from 24.5 to 23.7 mmol/L and increased chloride; urinary ammonium did not increase.
Potassium chloride → Plasma bicarbonate concentration source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Potassium salt/chloride -> acid-base balance.
experimental_model
Same two-week CKD cohort.
limitations
No randomized comparator; no significant blood-pressure or eGFR change.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
The chloride salt affected acid-base measurements as well as potassium.
primary_references
[k-gritter2022] Effects of Short-Term Potassium Chloride Supplementation in Patients with CKD (2022). https://pubmed.ncbi.nlm.nih.gov/35609996/ DOI: 10.1681/asn.2022020147
tissue_or_cell_type
Plasma and urine
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1650–1660
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Same two-week CKD cohort. · source_derived_draft · unverified_draft
### k-ckd-kcl-bicarbonate-response The same KCl run-in modestly lowered mean bicarbonate from 24.5 to 23.7 mmol/L and increased chloride; urinary ammonium did not increase. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The chloride salt affected acid-base measurements as well as potassium. organism: Homo sapiens tissue_or_cell_type: Plasma and urine experimental_model: Same two-week CKD cohort. limitations: No randomized comparator; no significant blood-pressure or eGFR change. cross_nutrient: Potassium salt/chloride -> acid-base balance. [k-gritter2022] Effects of Short-Term Potassium Chloride Supplementation in Patients with CKD (2022). https://pubmed.ncbi.nlm.nih.gov/35609996/ DOI: 10.1681/asn.2022020147
Complete structured claim and evidence
Bicarbonate salts and potassium gluconate increased bicarbonate in the CKD crossover; urinary citrate rose and ammonium fell.
Potassium bicarbonate → Plasma bicarbonate concentration source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Salt anion -> bicarbonate/citrate/ammonium.
experimental_model
31 participants; five-day randomized periods.
limitations
Short exposure and washout; unchanged diet advised rather than controlled.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
The accompanying anion changed the acid-base response.
primary_references
[k-ckd-salts2026] Randomized Cross-Over Trial of Electrolyte, Acid-Base and Blood Pressure Effects of Salt Supplements in CKD (2026). https://pubmed.ncbi.nlm.nih.gov/42381762/ DOI: 10.1016/j.ekir.2026.106619
tissue_or_cell_type
Plasma and urine
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1662–1672
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 31 participants; five-day randomized periods. · source_derived_draft · unverified_draft
### k-ckd-salts-alkalizing-comparison Bicarbonate salts and potassium gluconate increased bicarbonate in the CKD crossover; urinary citrate rose and ammonium fell. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The accompanying anion changed the acid-base response. organism: Homo sapiens tissue_or_cell_type: Plasma and urine experimental_model: 31 participants; five-day randomized periods. limitations: Short exposure and washout; unchanged diet advised rather than controlled. cross_nutrient: Salt anion -> bicarbonate/citrate/ammonium. [k-ckd-salts2026] Randomized Cross-Over Trial of Electrolyte, Acid-Base and Blood Pressure Effects of Salt Supplements in CKD (2026). https://pubmed.ncbi.nlm.nih.gov/42381762/ DOI: 10.1016/j.ekir.2026.106619
Complete structured claim and evidence
All three potassium salts increased plasma potassium despite their different acid-base effects.
Potassium ion → Plasma potassium concentration source_derived_draftungraded
Experimental context and source evidence
experimental_model
Same CKD crossover.
limitations
Cannot infer long-term food effects.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
An alkalizing potassium salt did not remove the potassium rise in this study.
primary_references
[k-ckd-salts2026] Randomized Cross-Over Trial of Electrolyte, Acid-Base and Blood Pressure Effects of Salt Supplements in CKD (2026). https://pubmed.ncbi.nlm.nih.gov/42381762/ DOI: 10.1016/j.ekir.2026.106619
tissue_or_cell_type
Plasma
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1674–1683
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Same CKD crossover. · source_derived_draft · unverified_draft
### k-ckd-salts-potassium-not-rescued-by-alkali All three potassium salts increased plasma potassium despite their different acid-base effects. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: An alkalizing potassium salt did not remove the potassium rise in this study. organism: Homo sapiens tissue_or_cell_type: Plasma experimental_model: Same CKD crossover. limitations: Cannot infer long-term food effects. [k-ckd-salts2026] Randomized Cross-Over Trial of Electrolyte, Acid-Base and Blood Pressure Effects of Salt Supplements in CKD (2026). https://pubmed.ncbi.nlm.nih.gov/42381762/ DOI: 10.1016/j.ekir.2026.106619
Complete structured claim and evidence
Potassium chloride and sodium chloride increased home systolic pressure versus placebo in the CKD crossover.
Potassium chloride → Arterial blood pressure source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Chloride salt/kidney context -> pressure.
experimental_model
Same five-day periods.
limitations
Context difference, not proof of a universal adverse potassium effect; molecular mediator unproven.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
The pressure response differed from trials in people with better kidney function.
primary_references
[k-ckd-salts2026] Randomized Cross-Over Trial of Electrolyte, Acid-Base and Blood Pressure Effects of Salt Supplements in CKD (2026). https://pubmed.ncbi.nlm.nih.gov/42381762/ DOI: 10.1016/j.ekir.2026.106619
tissue_or_cell_type
Systemic circulation
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1685–1695
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Same five-day periods. · source_derived_draft · unverified_draft
### k-ckd-chloride-salt-pressure Potassium chloride and sodium chloride increased home systolic pressure versus placebo in the CKD crossover. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The pressure response differed from trials in people with better kidney function. organism: Homo sapiens tissue_or_cell_type: Systemic circulation experimental_model: Same five-day periods. limitations: Context difference, not proof of a universal adverse potassium effect; molecular mediator unproven. cross_nutrient: Chloride salt/kidney context -> pressure. [k-ckd-salts2026] Randomized Cross-Over Trial of Electrolyte, Acid-Base and Blood Pressure Effects of Salt Supplements in CKD (2026). https://pubmed.ncbi.nlm.nih.gov/42381762/ DOI: 10.1016/j.ekir.2026.106619
Complete structured claim and evidence
The 75% NaCl/25% KCl salt substitute reduced stroke incidence versus ordinary salt in SSaSS (rate ratio 0.86).
Potassium chloride → Stroke incidence source_derived_draftungraded
Experimental context and source evidence
cross_nutrient
Combined sodium reduction/potassium increase; not potassium-alone molecular causation.
experimental_model
Cluster-randomized trial; mean 4.74-year follow-up.
limitations
Both sodium and potassium changed, so their effects cannot be separated. Serious kidney disease and potassium-sparing drugs/supplements were excluded; no serial serum-potassium surveillance.
nutrient_topic
Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
organism
Homo sapiens
plain_language
Replacing part of sodium chloride with potassium chloride improved a clinical outcome in the studied population.
primary_references
[k-neal2021] Effect of Salt Substitution on Cardiovascular Events and Death (2021). https://pubmed.ncbi.nlm.nih.gov/34459569/ DOI: 10.1056/nejmoa2105675
tissue_or_cell_type
Clinical cerebrovascular outcome
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1697–1707
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cluster-randomized trial; mean 4.74-year follow-up. · source_derived_draft · unverified_draft
### k-sodium-potassium-salt-stroke-trial The 75% NaCl/25% KCl salt substitute reduced stroke incidence versus ordinary salt in SSaSS (rate ratio 0.86). Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Replacing part of sodium chloride with potassium chloride improved a clinical outcome in the studied population. organism: Homo sapiens tissue_or_cell_type: Clinical cerebrovascular outcome experimental_model: Cluster-randomized trial; mean 4.74-year follow-up. limitations: Both sodium and potassium changed, so their effects cannot be separated. Serious kidney disease and potassium-sparing drugs/supplements were excluded; no serial serum-potassium surveillance. cross_nutrient: Combined sodium reduction/potassium increase; not potassium-alone molecular causation. [k-neal2021] Effect of Salt Substitution on Cardiovascular Events and Death (2021). https://pubmed.ncbi.nlm.nih.gov/34459569/ DOI: 10.1056/nejmoa2105675
Complete structured claim and evidence

Availability and dependencies

Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.

Low dietary potassium on a high-sodium background

Condition: nutrient_deficiency · Low dietary potassium on a high-sodium background

Normal role: The DCT adjusts sodium transport to potassium availability.

Recorded consequence: NCC activation can retain sodium while conserving potassium.

Scope: Mouse dietary experiments.

Adult renal Kcnj10 deletion

Condition: machinery_impairment · Adult renal Kcnj10 deletion

Normal role: Kir4.1 maintains DCT potassium conductance.

Recorded consequence: DCT depolarization and impaired potassium sensing.

Scope: Inducible knockout mice.

Kcnj16 deletion

Condition: machinery_impairment · Kcnj16 deletion

Normal role: Kir5.1 contributes to diet-responsive DCT conductance.

Recorded consequence: Loss of NCC adaptation and impaired whole-body K regulation.

Scope: Mouse genetic/diet model.

WNK4 L319F/L321F knockin

Condition: machinery_impairment · WNK4 L319F/L321F knockin Chloride-insensitive WNK4 expression

Normal role: WNK4 responds to intracellular chloride. WNK4 normally integrates chloride regulation.

Recorded consequence: NCC becomes insensitive to acute K loading. NCC remains phosphorylated during acute high-K challenge.

Scope: Mouse knockin. HEK expression experiment.

Engineered constitutively active SPAK with high-K adaptation

Condition: machinery_impairment · Engineered constitutively active SPAK with high-K adaptation

Normal role: Kinase/phosphatase balance controls NCC phosphorylation.

Recorded consequence: Adapted phosphatase regulation can suppress NCC despite constitutive kinase activity.

Scope: DCT-specific mouse transgenic model.

Dietary potassium restriction

Condition: nutrient_deficiency · Dietary potassium restriction

Normal role: Apical ROMK supports potassium secretion.

Recorded consequence: ROMK surface abundance falls.

Scope: Rat CCD imaging.

ROMK1-specific deletion during high-K feeding

Condition: machinery_impairment · ROMK1-specific deletion during high-K feeding

Normal role: ROMK1 contributes to secretory channel adaptation.

Recorded consequence: Blunted channel recruitment and elevated plasma K.

Scope: Mouse isoform-specific deletion.

Intercalated-cell Kcnma1 deletion

Condition: machinery_impairment · Intercalated-cell Kcnma1 deletion

Normal role: BK supports flow-responsive potassium secretion.

Recorded consequence: Isolated CCDs lose flow-induced K secretion.

Scope: High-K-adapted male and female mice.

Inducible renal mineralocorticoid-receptor deletion

Condition: machinery_impairment · Inducible renal mineralocorticoid-receptor deletion

Normal role: MR regulates distal sodium-channel function.

Recorded consequence: ENaC processing defect with salt wasting and hyperkalemia.

Scope: Adult mouse nephron deletion.

Renal tubular Sgk1 deletion during high-K feeding

Condition: machinery_impairment · Renal tubular Sgk1 deletion during high-K feeding

Normal role: SGK1 helps increase distal sodium-channel machinery.

Recorded consequence: Early potassium excretion defect and hyperkalemia.

Scope: Inducible mouse knockout.

Experimental depletion of intracellular potassium

Condition: nutrient_deficiency · Experimental depletion of intracellular potassium

Normal role: Cellular ion gradients support distal tubular magnesium entry.

Recorded consequence: Measured magnesium uptake falls.

Scope: Immortalized MDCT cells.

Low dietary K during high-NaCl feeding

Condition: nutrient_deficiency · Low dietary K during high-NaCl feeding

Normal role: Potassium availability participates in renal mineral handling.

Recorded consequence: Urinary calcium loss increases.

Scope: Male Dahl rat dietary comparison.

Prolonged experimental potassium depletion

Condition: nutrient_deficiency · Prolonged experimental potassium depletion

Normal role: Renal transport balances K secretion and reabsorption.

Recorded consequence: Potassium-selective absorptive adaptation increases.

Scope: Rat K/Rb clearance studies.

KCl versus placebo under a controlled dietary background

Condition: biomarker_context · KCl versus placebo under a controlled dietary background

Normal role: NCC participates in renal NaCl handling.

Recorded consequence: Urinary-vesicle NCC abundance falls.

Scope: Short crossover study in healthy adults.

Pan-Romk deletion

Condition: machinery_impairment · Pan-Romk deletion

Normal role: Apical potassium recycling supports loop salt absorption.

Recorded consequence: TAL NaCl absorption decreases.

Scope: Mouse knockout and segment-function experiments.

Low extracellular potassium in cardiac experiments

Condition: nutrient_deficiency · Acute bath-potassium reduction.

Normal role: Ion gradients support cell function.

Recorded consequence: Altered electrical and calcium handling.

Scope: Isolated cells/hearts; dietary cause not tested.

Reduced extracellular potassium and hERG

Condition: nutrient_deficiency · Low-K culture or rabbit K restriction.

Normal role: Ion gradients support cell function.

Recorded consequence: Less repolarizing channel availability.

Scope: Culture and animal dietary models remain distinct.

Whole-body potassium depletion and muscle transport

Condition: nutrient_deficiency · Dietary or pharmacological K depletion.

Normal role: Ion gradients support cell function.

Recorded consequence: Reduced muscle pump capacity.

Scope: Rodent depletion experiments.

Low potassium in inherited periodic-paralysis machinery

Condition: machinery_impairment · CACNA1S R528H plus low bath K.

Normal role: Ion gradients support cell function.

Recorded consequence: Depolarization-associated weakness.

Scope: Inherited channel defect; not dietary deficiency.

SUR1 nucleotide-regulatory impairment

Condition: machinery_impairment · Engineered SUR1 substitutions.

Normal role: Ion gradients support cell function.

Recorded consequence: Reduced MgADP activation.

Scope: Heterologous experiments.

Experimental potassium depletion and glucose handling

Condition: nutrient_deficiency · Restricted intake plus potassium-removal intervention.

Normal role: Ion gradients support cell function.

Recorded consequence: Altered insulin/glucose response.

Scope: Small human depletion studies.

Experimental cytosolic potassium loss

Condition: nutrient_deficiency · K-free medium after immune priming.

Normal role: Ion gradients support cell function.

Recorded consequence: Inflammasome activation.

Scope: Cellular ion perturbation, not malnutrition.

Potassium salts in glucose-intolerant adults

Condition: biomarker_context · Controlled oral supplementation.

Normal role: Ion gradients support cell function.

Recorded consequence: Glycemic endpoints tested.

Scope: Pilot trials; no prevention conclusion.

Potassium-dependent adaptation in renal proximal tubule and whole-kidney excretion

Condition: nutrient_deficiency · Rats on control or potassium-deficient diets for up to 6 days; NH4Cl co-loading and NRK52E/LLC-PK1 cell experiments.