Component

Ammonium ion

NH4+; distinct from uncharged NH3 and assays reporting their combined total.

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

Read recorded mechanisms Open recursive mind map

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

Where it participates (unsigned role)

  1. 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

  2. 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

  3. 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

  4. 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

  5. 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

  6. 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

  7. 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

In the sources

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

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