Component
Resting plasma-membrane potential
Resting plasma-membrane potential; interpretation depends on linked experimental context.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
Acute low-K superfusion hyperpolarized rat ventricular resting voltage despite increasing calcium transients.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- experimental_model
- Rat ventricular voltage and calcium recordings.
- limitations
- Do not equate hyperpolarization with protection from arrhythmia.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Rat
- plain_language
- A more negative resting voltage did not prevent calcium accumulation.
- primary_references
- [aronsen-2015-cardiac] Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase alpha2 activity (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4376427/ DOI: 10.1113/jphysiol.2014.279893
- tissue_or_cell_type
- Ventricle
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 634–643
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat ventricular voltage and calcium recordings. · source_derived_draft · unverified_draft
### k-low-cardiac-hyperpolarization Acute low-K superfusion hyperpolarized rat ventricular resting voltage despite increasing calcium transients. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A more negative resting voltage did not prevent calcium accumulation. organism: Rat tissue_or_cell_type: Ventricle experimental_model: Rat ventricular voltage and calcium recordings. limitations: Do not equate hyperpolarization with protection from arrhythmia. [aronsen-2015-cardiac] Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase alpha2 activity (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4376427/ DOI: 10.1113/jphysiol.2014.279893
Complete structured claim and evidence
Where it participates (unsigned role)
At 2 mM bath K, R528H muscle paradoxically depolarized and lost force while wild-type fibers hyperpolarized.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- A calcium-channel genetic defect changes potassium sensitivity of sodium-dependent muscle excitability.
- experimental_model
- 4.75 to 2 mM K challenge; mouse muscle recordings.
- limitations
- Sex/genotype influenced susceptibility; no general dietary-paralysis claim.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Mouse
- plain_language
- The same low-potassium exposure acted differently with inherited channel impairment.
- primary_references
- [wu-2012-hypopp] A calcium channel mutant mouse model of hypokalemic periodic paralysis (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3533564/ DOI: 10.1172/JCI66091
- tissue_or_cell_type
- Skeletal muscle
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 762–772
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 4.75 to 2 mM K challenge; mouse muscle recordings. · source_derived_draft · unverified_draft
### k-hypopp-low-k-depolarization At 2 mM bath K, R528H muscle paradoxically depolarized and lost force while wild-type fibers hyperpolarized. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same low-potassium exposure acted differently with inherited channel impairment. organism: Mouse tissue_or_cell_type: Skeletal muscle experimental_model: 4.75 to 2 mM K challenge; mouse muscle recordings. limitations: Sex/genotype influenced susceptibility; no general dietary-paralysis claim. cross_nutrient: A calcium-channel genetic defect changes potassium sensitivity of sodium-dependent muscle excitability. [wu-2012-hypopp] A calcium channel mutant mouse model of hypokalemic periodic paralysis (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3533564/ DOI: 10.1172/JCI66091
Complete structured claim and evidenceUntubulated atrial cells developed low-K early afterdepolarizations associated with sodium-current reactivation, hyperpolarization and brief action potentials.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- Low extracellular potassium changes sodium-channel availability in this cell population.
- experimental_model
- Rat atrial electrophysiology and modeling.
- limitations
- Distinct from the calcium-overload route in tubulated cells.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Rat
- plain_language
- Some atrial cells became unstable through sodium-channel behavior.
- primary_references
- [tazmini-2020-cardiac] Hypokalemia Promotes Arrhythmia by Distinct Mechanisms in Atrial and Ventricular Myocytes (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7098435/ DOI: 10.1161/CIRCRESAHA.119.315641
- tissue_or_cell_type
- Untubulated atrial myocytes
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 681–691
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat atrial electrophysiology and modeling. · source_derived_draft · unverified_draft
### k-low-atrial-sodium-reactivation Untubulated atrial cells developed low-K early afterdepolarizations associated with sodium-current reactivation, hyperpolarization and brief action potentials. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some atrial cells became unstable through sodium-channel behavior. organism: Rat tissue_or_cell_type: Untubulated atrial myocytes experimental_model: Rat atrial electrophysiology and modeling. limitations: Distinct from the calcium-overload route in tubulated cells. cross_nutrient: Low extracellular potassium changes sodium-channel availability in this cell population. [tazmini-2020-cardiac] Hypokalemia Promotes Arrhythmia by Distinct Mechanisms in Atrial and Ventricular Myocytes (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7098435/ DOI: 10.1161/CIRCRESAHA.119.315641
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.