Component

Aquaporin-2 / AQP2

Collecting duct water channel; total abundance is distinct from phosphorylation and membrane localization.

6 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

What acts on it

  1. 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

Where it participates (unsigned role)

  1. 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

  2. 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

  3. 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

  4. Amiloride increased maximal urine osmolality and AQP2 excretion in an eleven-patient crossover trial during lithium therapy.

    Amiloride → Human urine-concentrating response during lithium treatment source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Randomized placebo-controlled crossover; six-week periods.
    limitations
    Small trial; reduced lithium entry was inferred, not directly measured in patient kidney cells.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    Blocking a sodium channel improved the measured water response.
    primary_references
    Lithium-induced nephrogenic diabetes insipidus: renal effects of amiloride. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18596116/ · DOI 10.2215/CJN.01640408

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 344–350

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Randomized placebo-controlled crossover; six-week periods. · source_derived_draft · unverified_draft

    ## lithium-amiloride-human Blocking a sodium channel improved the measured water response. Amiloride increased maximal urine osmolality and AQP2 excretion in an eleven-patient crossover trial during lithium therapy. Model: Randomized placebo-controlled crossover; six-week periods. Limitations: Small trial; reduced lithium entry was inferred, not directly measured in patient kidney cells. Evidence access: Primary abstract Lithium-induced nephrogenic diabetes insipidus: renal effects of amiloride. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18596116/ · DOI 10.2215/CJN.01640408
    Complete structured claim and evidence

  5. Urine-concentrating impairment and lower urinary AQP2/cAMP correlated with lithium-treatment duration in patients.

    Lithium ion (Li+) → Human urine-concentrating response during lithium treatment source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    45 lithium-treated patients versus 42 on other psychotropics; desmopressin challenge.
    limitations
    Observational comparison cannot remove all confounding; urinary AQP2 is a marker, not a full tissue inventory.
    nutrient_topic
    Lithium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Lithium
    plain_language
    Human kidney findings connect the cellular route to water balance.
    primary_references
    Lithium-induced nephrogenic diabetes insipidus: renal effects of amiloride. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18596116/ · DOI 10.2215/CJN.01640408
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Lithium: metal-sensitive enzymes, transport and cross-nutrient mechanisms (2026-09-19) · lines 336–342

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 45 lithium-treated patients versus 42 on other psychotropics; desmopressin challenge. · source_derived_draft · unverified_draft

    ## lithium-human-concentration Human kidney findings connect the cellular route to water balance. Urine-concentrating impairment and lower urinary AQP2/cAMP correlated with lithium-treatment duration in patients. Model: 45 lithium-treated patients versus 42 on other psychotropics; desmopressin challenge. Limitations: Observational comparison cannot remove all confounding; urinary AQP2 is a marker, not a full tissue inventory. Evidence access: Primary abstract Lithium-induced nephrogenic diabetes insipidus: renal effects of amiloride. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18596116/ · DOI 10.2215/CJN.01640408
    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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