Component

Serum or plasma potassium concentration

Measured circulating potassium concentration; matrix is recorded in study context.

11 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Serum potassium rose after Mg repletion in both men studied during prolonged experimental Mg depletion.

    Magnesium → Serum or plasma potassium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    magnesium -> potassium
    experimental_model
    Within-person dietary depletion and repletion
    limitations
    Two elderly men; no native human channel assay and no causal localization of potassium loss to ROMK.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Homo sapiens
    plain_language
    Restoring Mg improved potassium status in these depleted individuals; the experiment does not show that every low potassium result has this cause.
    primary_references
    [shils-1964-human-depletion] Experimental Human Magnesium Depletion. I. Clinical Observations and Blood Chemistry Alterations (1964). https://pubmed.ncbi.nlm.nih.gov/14212747/ DOI: 10.1093/ajcn/15.3.133
    tissue_or_cell_type
    Blood and whole-body potassium pool
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 229–239

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Within-person dietary depletion and repletion · source_derived_draft · unverified_draft

    ### human-mg-repletion-restores-serum-k Serum potassium rose after Mg repletion in both men studied during prolonged experimental Mg depletion. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Restoring Mg improved potassium status in these depleted individuals; the experiment does not show that every low potassium result has this cause. organism: Homo sapiens tissue_or_cell_type: Blood and whole-body potassium pool experimental_model: Within-person dietary depletion and repletion limitations: Two elderly men; no native human channel assay and no causal localization of potassium loss to ROMK. cross_nutrient: magnesium -> potassium [shils-1964-human-depletion] Experimental Human Magnesium Depletion. I. Clinical Observations and Blood Chemistry Alterations (1964). https://pubmed.ncbi.nlm.nih.gov/14212747/ DOI: 10.1093/ajcn/15.3.133
    Complete structured claim and evidence
  2. Isolated Mg restriction produced hypomagnesemia without the hypokalemia observed under combined Na/Mg restriction in the tested mice.

    Magnesium → Serum or plasma potassium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    magnesium -> sodium -> potassium
    experimental_model
    Dietary restriction in C57BL/6J mice with renal transport assays
    limitations
    Model-specific non-sufficiency; not a claim that isolated Mg restriction can never lower K at other durations or in humans.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mus musculus
    plain_language
    A low Mg blood value alone did not guarantee falling potassium: sodium transport and the rest of the kidney response mattered.
    primary_references
    [maeoka-2025-enac-romk] Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK (2025). https://pubmed.ncbi.nlm.nih.gov/41137719/ DOI: 10.1113/JP287704
    tissue_or_cell_type
    Kidney distal nephron
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 166–176

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary restriction in C57BL/6J mice with renal transport assays · source_derived_draft · unverified_draft

    ### mg-restriction-alone-not-sufficient-hypokalemia Isolated Mg restriction produced hypomagnesemia without the hypokalemia observed under combined Na/Mg restriction in the tested mice. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A low Mg blood value alone did not guarantee falling potassium: sodium transport and the rest of the kidney response mattered. organism: Mus musculus tissue_or_cell_type: Kidney distal nephron experimental_model: Dietary restriction in C57BL/6J mice with renal transport assays limitations: Model-specific non-sufficiency; not a claim that isolated Mg restriction can never lower K at other durations or in humans. cross_nutrient: magnesium -> sodium -> potassium [maeoka-2025-enac-romk] Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK (2025). https://pubmed.ncbi.nlm.nih.gov/41137719/ DOI: 10.1113/JP287704
    Complete structured claim and evidence
  3. HCl infusion causing acute mineral acidemia raised plasma potassium in the conscious-dog experiment.

    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
  4. Beta-hydroxybutyric acid infusion lowered plasma potassium despite acidemia comparable to the HCl intervention.

    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
  5. The SSKI label warns of hyperkalemia with potassium-containing drugs, potassium-sparing diuretics or ACE inhibitors.

    Experimental context and source evidence
    experimental_model
    2025 SSKI manufacturer label; 1 g KI/mL formulation.
    exposure_category
    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.
    limitations
    Label warning, not a quantified primary interaction trial; applicability depends on exposure and patient context.
    nutrient_topic
    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide
    plain_language
    The potassium component matters when potassium excretion is impaired.
    primary_references
    SSKI product label, July 2025 · manufacturer label; DailyMed lists UNAPPROVED DRUG OTHER; not a trial or FDA approval · https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ca1d3449-ea29-49a4-8863-365ec95f1553

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 448–454

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · 2025 SSKI manufacturer label; 1 g KI/mL formulation. · source_derived_draft · unverified_draft

    ## ki-hyperkalemia The potassium component matters when potassium excretion is impaired. The SSKI label warns of hyperkalemia with potassium-containing drugs, potassium-sparing diuretics or ACE inhibitors. Model: 2025 SSKI manufacturer label; 1 g KI/mL formulation. Limitations: Label warning, not a quantified primary interaction trial; applicability depends on exposure and patient context. Evidence location: Primary abstract SSKI product label, July 2025 · manufacturer label; DailyMed lists UNAPPROVED DRUG OTHER; not a trial or FDA approval · https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ca1d3449-ea29-49a4-8863-365ec95f1553
    Complete structured claim and evidence
  6. On the experimental formula, men receiving 20.5 mEq/day potassium had serum potassium near the lower normal limit, while an extra 10.8 mEq/day maintained somewhat higher values across the paired B5 regimens.

    Experimental context and source evidence
    cross_nutrient
    true
    evidence_location
    Primary PDF pp.1643–1654; design, results and discussion.
    experimental_model
    Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls
    exposure
    Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium.
    limitations
    Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. No full potassium balance study was done; the record does not establish B5-dependent renal potassium wasting or refractory potassium repletion.
    nutrient_topic
    Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. · Pantothenate (vitamin B5)
    organism
    Homo sapiens
    plain_language
    Potassium supply affected the blood result independently of how the B5 groups were assigned.
    primary_references
    [b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756
    tissue_or_cell_type
    Whole-person symptoms, serum and urine

    Pantothenic acid (vitamin B5): coenzyme A, deficiency and nutrient interactions (2026-09-17) · lines 1187–1199

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls · source_derived_draft · unverified_draft

    ### b5-clin-potassium-context On the experimental formula, men receiving 20.5 mEq/day potassium had serum potassium near the lower normal limit, while an extra 10.8 mEq/day maintained somewhat higher values across the paired B5 regimens. Condition category: normal nutrient_topic: Pantothenic acid (vitamin B5) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium supply affected the blood result independently of how the B5 groups were assigned. organism: Homo sapiens tissue_or_cell_type: Whole-person symptoms, serum and urine experimental_model: Historical controlled feeding study in six adult male volunteers; two diet-only deficient, two deficient plus antagonist, two supplemented controls limitations: Very small historical cohort; other vitamins and formula composition were controlled imperfectly. Diet-only and antagonist groups are distinguished. Measurements do not establish a universal symptom, adrenal disease mechanism or cellular CoA threshold. No full potassium balance study was done; the record does not establish B5-dependent renal potassium wasting or refractory potassium repletion. exposure: Tube-fed experimental formula; controls received pantothenic acid 20 mg/day, antagonist pair 750 then 1000 mg/day omega-methyl compound; recovery included 4000 mg/day vitamin. One man per pair received 10.8 mEq/day extra potassium. cross_nutrient: true evidence_location: Primary PDF pp.1643–1654; design, results and discussion. [b5-clin-hodges1958] Pantothenic acid deficiency in man. (1958). https://pubmed.ncbi.nlm.nih.gov/13587673/ DOI: 10.1172/jci103756
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Combined Na/Mg restriction increased native ROMK activity in DCT2/CNT and lowered plasma K, while ENaC cleavage markers were preserved relative to normal diet.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    magnesium -> sodium -> potassium
    duration
    Seven days
    experimental_contrast
    {"combination": "joint", "comparator": "Normal diet", "conditions": [{"entity_slug": "sodium", "state": "Restricted"}, {"entity_slug": "magnesium", "state": "Restricted"}], "effect_direction": "increase", "endpoint": "Native ROMK activity in DCT2/CNT", "intervention": "Combined dietary sodium and magnesium restriction"} Primary abstract PMID 41137719 / DOI 10.1113/JP287704 rechecked 2026-09-20. This comparison must not be separated into two single-deficiency effects.
    experimental_model
    Dietary restriction in C57BL/6J mice with renal transport assays
    limitations
    Co-occurrence supports the proposed mechanism; intracellular Mg and distal Na delivery were not directly measured.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mus musculus
    plain_language
    In this combined shortage, the Mg-sensitive potassium pathway was more active while the sodium pathway that supports potassium exit remained available.
    primary_references
    [maeoka-2025-enac-romk] Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK (2025). https://pubmed.ncbi.nlm.nih.gov/41137719/ DOI: 10.1113/JP287704
    tissue_or_cell_type
    Kidney distal nephron
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 178–189

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary restriction in C57BL/6J mice with renal transport assays · source_derived_draft · unverified_draft

    ### combined-na-mg-restriction-romk-hypokalemia Combined Na/Mg restriction increased native ROMK activity in DCT2/CNT and lowered plasma K, while ENaC cleavage markers were preserved relative to normal diet. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this combined shortage, the Mg-sensitive potassium pathway was more active while the sodium pathway that supports potassium exit remained available. organism: Mus musculus tissue_or_cell_type: Kidney distal nephron experimental_model: Dietary restriction in C57BL/6J mice with renal transport assays limitations: Co-occurrence supports the proposed mechanism; intracellular Mg and distal Na delivery were not directly measured. cross_nutrient: magnesium -> sodium -> potassium duration: Seven days [maeoka-2025-enac-romk] Hypomagnesaemia-associated hypokalaemia requires activation of both ENaC and ROMK (2025). https://pubmed.ncbi.nlm.nih.gov/41137719/ DOI: 10.1113/JP287704
    Complete structured claim and evidence
  2. Prolonged experimental Mg depletion caused hypokalemia requiring substantial extra potassium intake to maintain serum K, alongside decreased exchangeable potassium.

    Magnesium → Potassium source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    magnesium -> potassium
    experimental_model
    Within-person dietary depletion and repletion
    limitations
    Two elderly men; no native human channel assay and no causal localization of potassium loss to ROMK.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Homo sapiens
    plain_language
    Supplying potassium became less effective at maintaining potassium status as Mg depletion progressed.
    primary_references
    [shils-1964-human-depletion] Experimental Human Magnesium Depletion. I. Clinical Observations and Blood Chemistry Alterations (1964). https://pubmed.ncbi.nlm.nih.gov/14212747/ DOI: 10.1093/ajcn/15.3.133
    tissue_or_cell_type
    Blood and whole-body potassium pool
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 217–227

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Within-person dietary depletion and repletion · source_derived_draft · unverified_draft

    ### human-mg-depletion-increases-k-replacement-needs Prolonged experimental Mg depletion caused hypokalemia requiring substantial extra potassium intake to maintain serum K, alongside decreased exchangeable potassium. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Supplying potassium became less effective at maintaining potassium status as Mg depletion progressed. organism: Homo sapiens tissue_or_cell_type: Blood and whole-body potassium pool experimental_model: Within-person dietary depletion and repletion limitations: Two elderly men; no native human channel assay and no causal localization of potassium loss to ROMK. cross_nutrient: magnesium -> potassium [shils-1964-human-depletion] Experimental Human Magnesium Depletion. I. Clinical Observations and Blood Chemistry Alterations (1964). https://pubmed.ncbi.nlm.nih.gov/14212747/ DOI: 10.1093/ajcn/15.3.133
    Complete structured claim and evidence
  3. Randomized additional Mg sulfate improved 48-hour potassium input-minus-urine balance in hypokalemic ICU adults despite similar serum K; between-group total potassium replacement was not significantly different.

    Magnesium → Potassium balance source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    cross_nutrient
    magnesium -> potassium
    experimental_model
    Double-blind placebo-controlled randomized surgical-ICU trial
    limitations
    Usual K/Mg treatment continued in both groups; 30 completers; hypokalemia enrollment did not establish intracellular Mg depletion in every patient.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Homo sapiens
    plain_language
    The Mg group retained more of the potassium supplied even though blood potassium looked similar. This supports retention, not a directly proven human ROMK mechanism.
    primary_references
    [hamill-ruth-1996-potassium-balance] Magnesium repletion and its effect on potassium homeostasis in critically ill adults: results of a double-blind, randomized, controlled trial. (1996). https://pubmed.ncbi.nlm.nih.gov/8565536/ DOI: 10.1097/00003246-199601000-00009
    tissue_or_cell_type
    Blood and timed urine collections
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 241–251

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind placebo-controlled randomized surgical-ICU trial · source_derived_draft · unverified_draft

    ### icu-mg-repletion-improves-potassium-balance Randomized additional Mg sulfate improved 48-hour potassium input-minus-urine balance in hypokalemic ICU adults despite similar serum K; between-group total potassium replacement was not significantly different. Condition category: biomarker_context nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The Mg group retained more of the potassium supplied even though blood potassium looked similar. This supports retention, not a directly proven human ROMK mechanism. organism: Homo sapiens tissue_or_cell_type: Blood and timed urine collections experimental_model: Double-blind placebo-controlled randomized surgical-ICU trial limitations: Usual K/Mg treatment continued in both groups; 30 completers; hypokalemia enrollment did not establish intracellular Mg depletion in every patient. cross_nutrient: magnesium -> potassium [hamill-ruth-1996-potassium-balance] Magnesium repletion and its effect on potassium homeostasis in critically ill adults: results of a double-blind, randomized, controlled trial. (1996). https://pubmed.ncbi.nlm.nih.gov/8565536/ DOI: 10.1097/00003246-199601000-00009
    Complete structured claim and evidence
  4. Four weeks of 0.1% versus 0.62% dietary K produced hypokalemia, reduced ventricular IKr and prolonged corrected QT in rabbits.

    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
  5. 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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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