Component

DCT membrane potential

Measured voltage across distal convoluted tubule cell membrane; sign and interventions specified per experiment.

4 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. Thiocyanate-induced hyperpolarization restored Mg2+ uptake in potassium-depleted MDCT cells.

    DCT membrane potential → Cellular magnesium influx source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    The K-depletion effect on Mg entry is partly recoverable by membrane polarization.
    evidence_location
    Primary abstract; SCN- rescue experiment.
    experimental_model
    SCN- voltage manipulation after cell K depletion
    limitations
    Supports partial voltage mediation; does not establish an in vivo repletion strategy.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mus musculus cell line
    plain_language
    Restoring the electrical driving force helped magnesium enter despite prior potassium depletion.
    primary_references
    [dai-1997-k-mg] Cellular mechanisms of chlorothiazide and cellular potassium depletion on Mg2+ uptake in mouse distal convoluted tubule cells (1997). https://pubmed.ncbi.nlm.nih.gov/9083264/ DOI: 10.1038/ki.1997.141
    tissue_or_cell_type
    Distal convoluted tubule cell model
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 497–508

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SCN- voltage manipulation after cell K depletion · source_derived_draft · unverified_draft

    ### renal-hyperpolarization-rescues-mg-after-k-depletion Thiocyanate-induced hyperpolarization restored Mg2+ uptake in potassium-depleted MDCT cells. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Restoring the electrical driving force helped magnesium enter despite prior potassium depletion. organism: Mus musculus cell line tissue_or_cell_type: Distal convoluted tubule cell model experimental_model: SCN- voltage manipulation after cell K depletion limitations: Supports partial voltage mediation; does not establish an in vivo repletion strategy. cross_nutrient: The K-depletion effect on Mg entry is partly recoverable by membrane polarization. evidence_location: Primary abstract; SCN- rescue experiment. [dai-1997-k-mg] Cellular mechanisms of chlorothiazide and cellular potassium depletion on Mg2+ uptake in mouse distal convoluted tubule cells (1997). https://pubmed.ncbi.nlm.nih.gov/9083264/ DOI: 10.1038/ki.1997.141
    Complete structured claim and evidence

What acts on it

  1. Adult renal Kir4.1 deletion depolarized DCT cells and abolished their voltage response to plasma potassium.

    Inward rectifier potassium channel Kir4.1 → DCT membrane potential source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Potassium conductance is needed to regulate apical sodium/chloride transport.
    evidence_location
    Abstract and Discussion; DCT patch-clamp experiments.
    experimental_model
    Inducible adult kidney-specific Kcnj10 deletion
    limitations
    Genetic loss is not dietary deficiency; Kir5.1 participation was not directly deleted in this study.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mus musculus
    plain_language
    Without Kir4.1, DCT cells lose the electrical response used to sense potassium.
    primary_references
    [cuevas-2017-kir4-sensing] Potassium Sensing by Renal Distal Tubules Requires Kir4.1 (2017). https://pmc.ncbi.nlm.nih.gov/articles/PMC5461801/ DOI: 10.1681/ASN.2016090935
    tissue_or_cell_type
    DCT basolateral membrane
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 190–201

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible adult kidney-specific Kcnj10 deletion · source_derived_draft · unverified_draft

    ### renal-kir4-loss-disables-sensing Adult renal Kir4.1 deletion depolarized DCT cells and abolished their voltage response to plasma potassium. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Without Kir4.1, DCT cells lose the electrical response used to sense potassium. organism: Mus musculus tissue_or_cell_type: DCT basolateral membrane experimental_model: Inducible adult kidney-specific Kcnj10 deletion limitations: Genetic loss is not dietary deficiency; Kir5.1 participation was not directly deleted in this study. cross_nutrient: Potassium conductance is needed to regulate apical sodium/chloride transport. evidence_location: Abstract and Discussion; DCT patch-clamp experiments. [cuevas-2017-kir4-sensing] Potassium Sensing by Renal Distal Tubules Requires Kir4.1 (2017). https://pmc.ncbi.nlm.nih.gov/articles/PMC5461801/ DOI: 10.1681/ASN.2016090935
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Potassium-depleted MDCT cells showed reduced Mg2+ uptake in a magnesium-recovery assay.

    Intracellular potassium content → Cellular magnesium influx source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Cellular K depletion decreases magnesium entry in this DCT model.
    evidence_location
    Primary abstract; potassium-depleted-cell Mg uptake comparison.
    experimental_model
    Cultured MDCT potassium depletion; fluorescence Mg-recovery assay
    limitations
    Intracellular depletion is distinct from low extracellular K alone; TRPM6 was not identified.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mus musculus cell line
    plain_language
    Depleting cellular potassium made it harder for these kidney cells to take up magnesium.
    primary_references
    [dai-1997-k-mg] Cellular mechanisms of chlorothiazide and cellular potassium depletion on Mg2+ uptake in mouse distal convoluted tubule cells (1997). https://pubmed.ncbi.nlm.nih.gov/9083264/ DOI: 10.1038/ki.1997.141
    tissue_or_cell_type
    Distal convoluted tubule cell model
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 484–495

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cultured MDCT potassium depletion; fluorescence Mg-recovery assay · source_derived_draft · unverified_draft

    ### renal-cellular-k-depletion-lowers-mg-influx Potassium-depleted MDCT cells showed reduced Mg2+ uptake in a magnesium-recovery assay. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Depleting cellular potassium made it harder for these kidney cells to take up magnesium. organism: Mus musculus cell line tissue_or_cell_type: Distal convoluted tubule cell model experimental_model: Cultured MDCT potassium depletion; fluorescence Mg-recovery assay limitations: Intracellular depletion is distinct from low extracellular K alone; TRPM6 was not identified. cross_nutrient: Cellular K depletion decreases magnesium entry in this DCT model. evidence_location: Primary abstract; potassium-depleted-cell Mg uptake comparison. [dai-1997-k-mg] Cellular mechanisms of chlorothiazide and cellular potassium depletion on Mg2+ uptake in mouse distal convoluted tubule cells (1997). https://pubmed.ncbi.nlm.nih.gov/9083264/ DOI: 10.1038/ki.1997.141
    Complete structured claim and evidence

  2. Low-K medium lowered intracellular chloride in HEK293 and mDCT cells; depolarizing Kir4.1 mutants increased it.

    Potassium ion → Intracellular chloride concentration source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Extracellular K controls the intracellular chloride signal.
    evidence_location
    Figure 6A-B; Figure S5.
    experimental_model
    Cell culture and Kir4.1 mutant comparisons
    limitations
    HEK chloride and WNK expression differ from native DCT.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Homo sapiens; Mus musculus cell lines
    plain_language
    A change outside the cell can change chloride inside, connecting potassium sensing to salt transport.
    primary_references
    [terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006
    tissue_or_cell_type
    HEK293 and mDCT cells

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 125–136

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell culture and Kir4.1 mutant comparisons · source_derived_draft · unverified_draft

    ### renal-low-external-k-lowers-cell-chloride Low-K medium lowered intracellular chloride in HEK293 and mDCT cells; depolarizing Kir4.1 mutants increased it. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A change outside the cell can change chloride inside, connecting potassium sensing to salt transport. organism: Homo sapiens; Mus musculus cell lines tissue_or_cell_type: HEK293 and mDCT cells experimental_model: Cell culture and Kir4.1 mutant comparisons limitations: HEK chloride and WNK expression differ from native DCT. cross_nutrient: Extracellular K controls the intracellular chloride signal. evidence_location: Figure 6A-B; Figure S5. [terker-2015-k-voltage-chloride] Potassium Modulates Electrolyte Balance and Blood Pressure through Effects on Distal Cell Voltage and Chloride (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4332769/ DOI: 10.1016/j.cmet.2014.12.006
    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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