Component

ENaC-mediated sodium current

ENaC-mediated sodium current. Species, exposure and limitations are retained in each linked 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 acts on it

  1. The alpha- or beta-subunit variants identified in affected families caused loss of channel activity.

    Epithelial sodium channel → ENaC-mediated sodium current source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/8589714.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e", "start_char": 0, "end_char": 696, "text_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e"}
    experimental_model
    Human family genetics and sodium-channel functional testing
    exposure
    Loss-of-function alpha- or beta-subunit variants in five kindreds
    limitations
    Autosomal recessive pseudohypoaldosteronism; not ordinary dietary sodium deficiency and not proof that additional aldosterone can repair the channel.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Human
    plain_language
    The sodium entry channel itself can fail.
    primary_references
    [sodium-p8589714] Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1. (1996). https://pubmed.ncbi.nlm.nih.gov/8589714/ DOI: 10.1038/ng0396-248
    tissue_or_cell_type
    ENaC-dependent epithelia and systemic electrolyte phenotype
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 928–939

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human family genetics and sodium-channel functional testing · source_derived_draft · unverified_draft

    ### sodium-enac-loss-current The alpha- or beta-subunit variants identified in affected families caused loss of channel activity. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The sodium entry channel itself can fail. organism: Human tissue_or_cell_type: ENaC-dependent epithelia and systemic electrolyte phenotype experimental_model: Human family genetics and sodium-channel functional testing limitations: Autosomal recessive pseudohypoaldosteronism; not ordinary dietary sodium deficiency and not proof that additional aldosterone can repair the channel. exposure: Loss-of-function alpha- or beta-subunit variants in five kindreds evidence_span: {"source_cache": "artifacts/sodium-research/8589714.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e", "start_char": 0, "end_char": 696, "text_sha256": "c85f54f2086e1dc34cabaa8e4521a157bfeb5512b7882ca214ddfa2597b9bc4e"} [sodium-p8589714] Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1. (1996). https://pubmed.ncbi.nlm.nih.gov/8589714/ DOI: 10.1038/ng0396-248
    Complete structured claim and evidence

  2. The beta-subunit P616L mutant increased amiloride-sensitive sodium current 8.8-fold versus normal subunits in oocytes.

    Human ENaC beta-subunit P616L variant as numbered in the 1995 study → ENaC-mediated sodium current source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/8524790.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "31f8bb4c6f32108b9d6042db6ec60ed8c77b21af322621a2cb0fd9c2aa7236a1", "start_char": 0, "end_char": 1598, "text_sha256": "31f8bb4c6f32108b9d6042db6ec60ed8c77b21af322621a2cb0fd9c2aa7236a1"}
    experimental_model
    Human kindred analysis and oocyte channel-expression comparison
    exposure
    P616L as numbered in the paper
    limitations
    Gain-of-function genetic disease; no implication that this mutation is caused by salt intake.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Human variant in Xenopus oocytes
    plain_language
    A mutation can make sodium entry excessive even without a defective sodium supply.
    primary_references
    [sodium-p8524790] A de novo missense mutation of the beta subunit of the epithelial sodium channel causes hypertension and Liddle syndrome, identifying a proline-rich segment critical for regulation of channel activity. (1995). https://pubmed.ncbi.nlm.nih.gov/8524790/ DOI: 10.1073/pnas.92.25.11495
    tissue_or_cell_type
    ENaC beta-subunit regulatory tail
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 954–965

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human kindred analysis and oocyte channel-expression comparison · source_derived_draft · unverified_draft

    ### sodium-liddle-current The beta-subunit P616L mutant increased amiloride-sensitive sodium current 8.8-fold versus normal subunits in oocytes. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A mutation can make sodium entry excessive even without a defective sodium supply. organism: Human variant in Xenopus oocytes tissue_or_cell_type: ENaC beta-subunit regulatory tail experimental_model: Human kindred analysis and oocyte channel-expression comparison limitations: Gain-of-function genetic disease; no implication that this mutation is caused by salt intake. exposure: P616L as numbered in the paper evidence_span: {"source_cache": "artifacts/sodium-research/8524790.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "31f8bb4c6f32108b9d6042db6ec60ed8c77b21af322621a2cb0fd9c2aa7236a1", "start_char": 0, "end_char": 1598, "text_sha256": "31f8bb4c6f32108b9d6042db6ec60ed8c77b21af322621a2cb0fd9c2aa7236a1"} [sodium-p8524790] A de novo missense mutation of the beta subunit of the epithelial sodium channel causes hypertension and Liddle syndrome, identifying a proline-rich segment critical for regulation of channel activity. (1995). https://pubmed.ncbi.nlm.nih.gov/8524790/ DOI: 10.1073/pnas.92.25.11495
    Complete structured claim and evidence

  3. Coexpression of mouse sgk with the three ENaC subunits increased sodium current in Xenopus oocytes.

    Serum and glucocorticoid-regulated kinase 1 → ENaC-mediated sodium current 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
    The kinase can increase sodium flow through ENaC.
    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 408–419

    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-sgk-enac Coexpression of mouse sgk with the three ENaC subunits increased sodium current in Xenopus oocytes. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kinase can increase sodium flow through ENaC. 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

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