Component

Mineralocorticoid receptor

Canonical protein; experimental species, state, expression context and nutritional dependence are specified per claim.

3 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 it acts on

  1. 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

Where it participates (unsigned role)

  1. Aldosterone increased collecting-duct sgk mRNA within 30 minutes through mineralocorticoid receptors without requiring new protein synthesis.

    Aldosterone → SGK1 transcript and protein expression source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sodium-research/10358046.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b", "start_char": 0, "end_char": 1343, "text_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b"}
    experimental_model
    Immediate-early gene induction and channel coexpression
    exposure
    Aldosterone exposure; receptor dependence and protein-synthesis tests
    limitations
    Cell and oocyte mechanism; the study does not imply that dietary sodium directly activates SGK1 in every tissue.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Rabbit/mouse collecting-duct preparations; mouse SGK in Xenopus oocytes
    plain_language
    A hormone can quickly increase the instructions for a kinase that regulates sodium transport.
    primary_references
    [sodium-p10358046] sgk is an aldosterone-induced kinase in the renal collecting duct. Effects on epithelial na+ channels. (1999). https://pubmed.ncbi.nlm.nih.gov/10358046/ DOI: 10.1074/jbc.274.24.16973
    tissue_or_cell_type
    Cortical collecting duct and expression system

    Sodium: gradients, nutrient transport, fluid regulation and loss states (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 · Immediate-early gene induction and channel coexpression · source_derived_draft · unverified_draft

    ### sodium-aldosterone-sgk Aldosterone increased collecting-duct sgk mRNA within 30 minutes through mineralocorticoid receptors without requiring new protein synthesis. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A hormone can quickly increase the instructions for a kinase that regulates sodium transport. organism: Rabbit/mouse collecting-duct preparations; mouse SGK in Xenopus oocytes tissue_or_cell_type: Cortical collecting duct and expression system experimental_model: Immediate-early gene induction and channel coexpression limitations: Cell and oocyte mechanism; the study does not imply that dietary sodium directly activates SGK1 in every tissue. exposure: Aldosterone exposure; receptor dependence and protein-synthesis tests evidence_span: {"source_cache": "artifacts/sodium-research/10358046.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b", "start_char": 0, "end_char": 1343, "text_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b"} [sodium-p10358046] sgk is an aldosterone-induced kinase in the renal collecting duct. Effects on epithelial na+ channels. (1999). https://pubmed.ncbi.nlm.nih.gov/10358046/ DOI: 10.1074/jbc.274.24.16973
    Complete structured claim and evidence

  2. 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

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