Component

Amiloride

ENaC inhibitor used experimentally to probe renal sodium transport.

3 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 it acts on

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

    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

Where it participates (unsigned role)

  1. Mg restriction reduced cleaved alpha/gamma ENaC abundance and blunted amiloride-induced sodium excretion in mice.

    Magnesium → Epithelial sodium channel 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
    Cleaved subunits and amiloride response support ENaC inhibition; the molecular cause was unresolved.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Mus musculus
    plain_language
    With less dietary Mg, these kidneys reduced the sodium entry pathway that normally helps drive potassium secretion.
    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 154–164

    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-reduces-enac-activity Mg restriction reduced cleaved alpha/gamma ENaC abundance and blunted amiloride-induced sodium excretion in mice. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: With less dietary Mg, these kidneys reduced the sodium entry pathway that normally helps drive potassium secretion. organism: Mus musculus tissue_or_cell_type: Kidney distal nephron experimental_model: Dietary restriction in C57BL/6J mice with renal transport assays limitations: Cleaved subunits and amiloride response support ENaC inhibition; the molecular cause was unresolved. 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
  2. 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

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.

    Evidence, AI assistance and curation standards