Component

Large-conductance calcium-activated potassium channel alpha subunit

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

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 it acts on

  1. Patients with end-stage renal disease showed higher colonic BK expression and approximately threefold higher rectal potassium secretion than controls.

    Large-conductance calcium-activated potassium channel alpha subunit → Colonic potassium secretion source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Kidney failure -> extra-renal potassium handling.
    experimental_model
    Small human biopsy and rectal-dialysis groups.
    limitations
    Expression plus association does not identify every flux pathway; no diet intervention.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Homo sapiens
    plain_language
    The colon can increase its potassium-disposal role when kidney function is severely reduced.
    primary_references
    [k-sandle2005] Enhanced large intestinal potassium permeability in end-stage renal disease (2005). https://pubmed.ncbi.nlm.nih.gov/15772943/ DOI: 10.1002/path.1750
    tissue_or_cell_type
    Human distal colon and rectum

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1475–1485

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Small human biopsy and rectal-dialysis groups. · source_derived_draft · unverified_draft

    ### k-esrd-colonic-bk-upregulation Patients with end-stage renal disease showed higher colonic BK expression and approximately threefold higher rectal potassium secretion than controls. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The colon can increase its potassium-disposal role when kidney function is severely reduced. organism: Homo sapiens tissue_or_cell_type: Human distal colon and rectum experimental_model: Small human biopsy and rectal-dialysis groups. limitations: Expression plus association does not identify every flux pathway; no diet intervention. cross_nutrient: Kidney failure -> extra-renal potassium handling. [k-sandle2005] Enhanced large intestinal potassium permeability in end-stage renal disease (2005). https://pubmed.ncbi.nlm.nih.gov/15772943/ DOI: 10.1002/path.1750
    Complete structured claim and evidence

  2. Intercalated-cell BKalpha deletion abolished flow-stimulated K secretion in isolated mouse CCDs from both sexes.

    Large-conductance calcium-activated potassium channel alpha subunit → Distal renal potassium secretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    A calcium-activated K channel connects tubular flow to K elimination.
    evidence_location
    Figure 5; sex context Figure 8.
    experimental_model
    Cell-specific knockout; high-K adaptation; microperfusion
    limitations
    Chronic blood K elevation occurred only in males; whole-animal urinary outputs showed compensation.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mus musculus
    plain_language
    Flow-dependent potassium secretion needs BK channels in intercalated cells.
    primary_references
    [carrisoza-2020-intercalated-bk] Intercalated cell BKalpha subunit is required for flow-induced K+ secretion (2020). https://insight.jci.org/articles/view/130553 DOI: 10.1172/jci.insight.130553
    tissue_or_cell_type
    CCD intercalated cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 356–367

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-specific knockout; high-K adaptation; microperfusion · source_derived_draft · unverified_draft

    ### renal-intercalated-bk-flow-secretion Intercalated-cell BKalpha deletion abolished flow-stimulated K secretion in isolated mouse CCDs from both sexes. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Flow-dependent potassium secretion needs BK channels in intercalated cells. organism: Mus musculus tissue_or_cell_type: CCD intercalated cells experimental_model: Cell-specific knockout; high-K adaptation; microperfusion limitations: Chronic blood K elevation occurred only in males; whole-animal urinary outputs showed compensation. cross_nutrient: A calcium-activated K channel connects tubular flow to K elimination. evidence_location: Figure 5; sex context Figure 8. [carrisoza-2020-intercalated-bk] Intercalated cell BKalpha subunit is required for flow-induced K+ secretion (2020). https://insight.jci.org/articles/view/130553 DOI: 10.1172/jci.insight.130553
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Luminal barium reduced potassium secretion by about 45% in the kidney-failure group, supporting a potassium-channel contribution.

    Barium ion → Colonic potassium secretion source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Rectal dialysis with 5 mmol/L barium.
    limitations
    Barium is not BK-specific; combine this with expression evidence without asserting exclusive BK mediation.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Homo sapiens
    plain_language
    Part of the extra gut potassium loss depended on a blocker-sensitive pathway.
    primary_references
    [k-sandle2005] Enhanced large intestinal potassium permeability in end-stage renal disease (2005). https://pubmed.ncbi.nlm.nih.gov/15772943/ DOI: 10.1002/path.1750
    tissue_or_cell_type
    Human rectum

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1487–1496

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rectal dialysis with 5 mmol/L barium. · source_derived_draft · unverified_draft

    ### k-esrd-colonic-barium-sensitive-secretion Luminal barium reduced potassium secretion by about 45% in the kidney-failure group, supporting a potassium-channel contribution. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Part of the extra gut potassium loss depended on a blocker-sensitive pathway. organism: Homo sapiens tissue_or_cell_type: Human rectum experimental_model: Rectal dialysis with 5 mmol/L barium. limitations: Barium is not BK-specific; combine this with expression evidence without asserting exclusive BK mediation. [k-sandle2005] Enhanced large intestinal potassium permeability in end-stage renal disease (2005). https://pubmed.ncbi.nlm.nih.gov/15772943/ DOI: 10.1002/path.1750
    Complete structured claim and evidence

  2. Marked BK overexpression accompanied colonic potassium-secretory diarrhea and hypokalemia in the reported patient.

    Colonic BK channel abundance → Colonic potassium secretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    Single case; symptoms resolved after colectomy.
    limitations
    The proposed shock/ischemia-to-BK chain remains a hypothesis.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Homo sapiens
    plain_language
    Severe potassium loss can occur through the gut even in kidney failure.
    primary_references
    [k-van-dinter2008] Over-expression of colonic K+ channels associated with severe potassium secretory diarrhoea after haemorrhagic shock (2008). https://pubmed.ncbi.nlm.nih.gov/18653901/ DOI: 10.1093/ndt/gfn411
    tissue_or_cell_type
    Human colon
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1498–1507

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single case; symptoms resolved after colectomy. · source_derived_draft · unverified_draft

    ### k-secretory-diarrhea-bk-case Marked BK overexpression accompanied colonic potassium-secretory diarrhea and hypokalemia in the reported patient. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Severe potassium loss can occur through the gut even in kidney failure. organism: Homo sapiens tissue_or_cell_type: Human colon experimental_model: Single case; symptoms resolved after colectomy. limitations: The proposed shock/ischemia-to-BK chain remains a hypothesis. [k-van-dinter2008] Over-expression of colonic K+ channels associated with severe potassium secretory diarrhoea after haemorrhagic shock (2008). https://pubmed.ncbi.nlm.nih.gov/18653901/ DOI: 10.1093/ndt/gfn411
    Complete structured claim and evidence

  3. Removing luminal Ca2+ or buffering intracellular Ca2+ suppressed flow-stimulated K secretion in microperfused rabbit CCDs.

    Calcium ion → Distal renal potassium secretion source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Local calcium availability permits flow-stimulated potassium secretion.
    evidence_location
    Results; luminal Ca and intracellular buffering experiments.
    experimental_model
    Luminal Ca removal/BAPTA and flow challenge
    limitations
    Tests ion availability in vitro, not dietary calcium deficiency; the entry-channel identity was unresolved.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Oryctolagus cuniculus
    plain_language
    Calcium entry and signaling are required for this flow-driven potassium output.
    primary_references
    [liu-2007-calcium-flow] Ca2+ dependence of flow-stimulated K secretion in the mammalian cortical collecting duct (2007). https://journals.physiology.org/doi/10.1152/ajprenal.00057.2007 DOI: 10.1152/ajprenal.00057.2007
    tissue_or_cell_type
    Cortical collecting duct

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 369–380

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Luminal Ca removal/BAPTA and flow challenge · source_derived_draft · unverified_draft

    ### renal-calcium-entry-supports-flow-k-secretion Removing luminal Ca2+ or buffering intracellular Ca2+ suppressed flow-stimulated K secretion in microperfused rabbit CCDs. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium entry and signaling are required for this flow-driven potassium output. organism: Oryctolagus cuniculus tissue_or_cell_type: Cortical collecting duct experimental_model: Luminal Ca removal/BAPTA and flow challenge limitations: Tests ion availability in vitro, not dietary calcium deficiency; the entry-channel identity was unresolved. cross_nutrient: Local calcium availability permits flow-stimulated potassium secretion. evidence_location: Results; luminal Ca and intracellular buffering experiments. [liu-2007-calcium-flow] Ca2+ dependence of flow-stimulated K secretion in the mammalian cortical collecting duct (2007). https://journals.physiology.org/doi/10.1152/ajprenal.00057.2007 DOI: 10.1152/ajprenal.00057.2007
    Complete structured claim and evidence

  4. An alcohol-sensing site was identified in the calcium- and voltage-gated large conductance potassium channel.

    Ethanol → Large-conductance calcium- and voltage-gated potassium (BK) channel source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/alcohol-research/24927535.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ef6f89212505affcd872cd85809dfd8f4036b04e6d3a86b2b24a3b5bdc33f706", "start_char": 0, "end_char": 1201, "text_sha256": "ef6f89212505affcd872cd85809dfd8f4036b04e6d3a86b2b24a3b5bdc33f706"}
    experimental_model
    Structure-function mapping of the BK channel cytosolic gating ring
    exposure
    Alcohol applied to defined channel constructs
    limitations
    Identifies a discrete alcohol-sensing site. A site in a recombinant channel is not proof that occupancy explains an intact behaviour.
    nutrient_topic
    Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
    organism
    Recombinant channel
    plain_language
    Alcohol has a physical docking place on this potassium channel.
    primary_references
    [alcohol-p24927535] An alcohol-sensing site in the calcium- and voltage-gated, large conductance potassium (BK) channel. (2014). https://pubmed.ncbi.nlm.nih.gov/24927535/ DOI: 10.1073/pnas.1317363111
    tissue_or_cell_type
    BK channel

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 358–369

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Structure-function mapping of the BK channel cytosolic gating ring · source_derived_draft · unverified_draft

    ### alcohol-bk-alcohol-site An alcohol-sensing site was identified in the calcium- and voltage-gated large conductance potassium channel. Condition category: normal nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: Alcohol has a physical docking place on this potassium channel. organism: Recombinant channel tissue_or_cell_type: BK channel experimental_model: Structure-function mapping of the BK channel cytosolic gating ring limitations: Identifies a discrete alcohol-sensing site. A site in a recombinant channel is not proof that occupancy explains an intact behaviour. exposure: Alcohol applied to defined channel constructs evidence_span: {"source_cache": "artifacts/alcohol-research/24927535.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "ef6f89212505affcd872cd85809dfd8f4036b04e6d3a86b2b24a3b5bdc33f706", "start_char": 0, "end_char": 1201, "text_sha256": "ef6f89212505affcd872cd85809dfd8f4036b04e6d3a86b2b24a3b5bdc33f706"} [alcohol-p24927535] An alcohol-sensing site in the calcium- and voltage-gated, large conductance potassium (BK) channel. (2014). https://pubmed.ncbi.nlm.nih.gov/24927535/ DOI: 10.1073/pnas.1317363111
    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