Component

Extracellular potassium concentration

Extracellular potassium concentration; interpretation depends on linked experimental context.

8 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. Raising extracellular K to 45 mM maximally inhibited NLRP3 responses to the tested toxins and particles.

    Extracellular potassium concentration → NLRP3 inflammasome source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Primed mouse macrophages, extracellular-K titration.
    exposure
    Artificial extracellular potassium elevation; not dietary excess.
    limitations
    Stimulus-specific; does not justify elevating blood potassium.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mouse
    plain_language
    Reducing the outward potassium gradient blocked these activation routes.
    primary_references
    [munoz-2013-nlrp3] K+ efflux is the Common Trigger of NLRP3 inflammasome Activation by Bacterial Toxins and Particulate Matter (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3730833/ DOI: 10.1016/j.immuni.2013.05.016
    tissue_or_cell_type
    Bone-marrow macrophages

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 868–878

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primed mouse macrophages, extracellular-K titration. · source_derived_draft · unverified_draft

    ### k-high-medium-nlrp3-block Raising extracellular K to 45 mM maximally inhibited NLRP3 responses to the tested toxins and particles. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reducing the outward potassium gradient blocked these activation routes. organism: Mouse tissue_or_cell_type: Bone-marrow macrophages experimental_model: Primed mouse macrophages, extracellular-K titration. limitations: Stimulus-specific; does not justify elevating blood potassium. exposure: Artificial extracellular potassium elevation; not dietary excess. [munoz-2013-nlrp3] K+ efflux is the Common Trigger of NLRP3 inflammasome Activation by Bacterial Toxins and Particulate Matter (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3730833/ DOI: 10.1016/j.immuni.2013.05.016
    Complete structured claim and evidence

  2. Rabbit hearts exposed to 2.7 mM K showed increased CaMKII activity; KN-93 prevented low-K early afterdepolarizations and ventricular arrhythmia.

    Extracellular potassium concentration → Ca2+/calmodulin-dependent protein kinase II family source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Potassium depletion of the bath alters calcium-dependent signaling.
    experimental_model
    Isolated hearts; enzyme assay and inhibitor intervention.
    limitations
    Pharmacology is not genetic specificity; clinical efficacy was not tested.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Rabbit and rat experimental series
    plain_language
    Calcium-sensitive kinase signaling contributed to electrical instability.
    primary_references
    [pezhouman-2015-camkii] Molecular Basis of Hypokalemia-Induced Ventricular Fibrillation (2015). https://pubmed.ncbi.nlm.nih.gov/26269574/ DOI: 10.1161/CIRCULATIONAHA.115.016217
    tissue_or_cell_type
    Ventricular myocardium
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 645–655

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated hearts; enzyme assay and inhibitor intervention. · source_derived_draft · unverified_draft

    ### k-low-activates-camkii Rabbit hearts exposed to 2.7 mM K showed increased CaMKII activity; KN-93 prevented low-K early afterdepolarizations and ventricular arrhythmia. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium-sensitive kinase signaling contributed to electrical instability. organism: Rabbit and rat experimental series tissue_or_cell_type: Ventricular myocardium experimental_model: Isolated hearts; enzyme assay and inhibitor intervention. limitations: Pharmacology is not genetic specificity; clinical efficacy was not tested. cross_nutrient: Potassium depletion of the bath alters calcium-dependent signaling. [pezhouman-2015-camkii] Molecular Basis of Hypokalemia-Induced Ventricular Fibrillation (2015). https://pubmed.ncbi.nlm.nih.gov/26269574/ DOI: 10.1161/CIRCULATIONAHA.115.016217
    Complete structured claim and evidence

  3. Untubulated atrial cells developed low-K early afterdepolarizations associated with sodium-current reactivation, hyperpolarization and brief action potentials.

    Extracellular potassium concentration → Cardiac early afterdepolarizations source_derived_draftungraded
    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

  4. Low-K exposure increased calcium waves in ventricular and tubulated atrial cells, with a weaker response in untubulated atrial cells.

    Extracellular potassium concentration → Propagating cardiac calcium waves source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    The calcium response to potassium depends on cellular transport organization.
    experimental_model
    Rat myocytes, 5.0 to 2.7 mM K, 3 minutes.
    limitations
    Architecture-dependent findings should not be generalized to all heart cells.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Rat
    plain_language
    Internal membrane architecture changed how low potassium disturbed calcium.
    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
    Atrial/ventricular myocardium
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 669–679

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat myocytes, 5.0 to 2.7 mM K, 3 minutes. · source_derived_draft · unverified_draft

    ### k-low-calcium-waves-tubules Low-K exposure increased calcium waves in ventricular and tubulated atrial cells, with a weaker response in untubulated atrial cells. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Internal membrane architecture changed how low potassium disturbed calcium. organism: Rat tissue_or_cell_type: Atrial/ventricular myocardium experimental_model: Rat myocytes, 5.0 to 2.7 mM K, 3 minutes. limitations: Architecture-dependent findings should not be generalized to all heart cells. cross_nutrient: The calcium response to potassium depends on cellular transport organization. [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

  5. Acute low-K superfusion hyperpolarized rat ventricular resting voltage despite increasing calcium transients.

    Extracellular potassium concentration → Resting plasma-membrane potential source_derived_draftungraded
    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

  6. Lowering bath K from 5.0 to 2.7 mM reduced ventricular pump current and increased intracellular sodium.

    Extracellular potassium concentration → Sodium-potassium ATPase complexes source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Low extracellular potassium compromises sodium extrusion.
    experimental_model
    Rat ventricular patch clamp/Na fluorescence.
    limitations
    Acute bath manipulation; not dietary depletion.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Rat
    plain_language
    With less extracellular potassium, sodium extrusion slowed.
    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
    Ventricular myocytes
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 610–620

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat ventricular patch clamp/Na fluorescence. · source_derived_draft · unverified_draft

    ### k-low-cardiac-pump-current Lowering bath K from 5.0 to 2.7 mM reduced ventricular pump current and increased intracellular sodium. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: With less extracellular potassium, sodium extrusion slowed. organism: Rat tissue_or_cell_type: Ventricular myocytes experimental_model: Rat ventricular patch clamp/Na fluorescence. limitations: Acute bath manipulation; not dietary depletion. cross_nutrient: Low extracellular potassium compromises sodium extrusion. [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

  7. Low extracellular K accelerated hERG internalization and degradation; 0 versus 5 mM exposure strongly reduced mature surface channels.

    Extracellular potassium concentration → Cell-surface hERG abundance source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    Transfected HEK293 cells, 6-12-hour low-K exposures.
    limitations
    Zero-K culture is more extreme than ordinary hypokalemia.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Human protein in HEK293 cells
    plain_language
    Potassium outside the cell helped retain a cardiac repolarizing channel.
    primary_references
    [guo-2009-herg] Extracellular K+ concentration controls cell surface density of IKr in rabbit hearts and of the HERG channel in human cell lines (2009). https://www.jci.org/articles/view/39027 DOI: 10.1172/JCI39027
    tissue_or_cell_type
    Heterologous culture
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 693–702

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected HEK293 cells, 6-12-hour low-K exposures. · source_derived_draft · unverified_draft

    ### k-low-herg-turnover Low extracellular K accelerated hERG internalization and degradation; 0 versus 5 mM exposure strongly reduced mature surface channels. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium outside the cell helped retain a cardiac repolarizing channel. organism: Human protein in HEK293 cells tissue_or_cell_type: Heterologous culture experimental_model: Transfected HEK293 cells, 6-12-hour low-K exposures. limitations: Zero-K culture is more extreme than ordinary hypokalemia. [guo-2009-herg] Extracellular K+ concentration controls cell surface density of IKr in rabbit hearts and of the HERG channel in human cell lines (2009). https://www.jci.org/articles/view/39027 DOI: 10.1172/JCI39027
    Complete structured claim and evidence

  8. The combined 85 mM Na/9 mM K bath reduced M-wave area and tetanic force versus 147 mM Na/4 mM K.

    Extracellular potassium concentration → Skeletal muscle excitability source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Reduced sodium and elevated potassium jointly impair excitability.
    experimental_model
    Isolated rat soleus, combined bath-ion perturbation.
    limitations
    Combined perturbation cannot be attributed to potassium alone; not dietary excess.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Rat
    plain_language
    Both sodium and potassium gradients matter for muscle activation.
    primary_references
    [overgaard-1999-muscle] Relations between excitability and contractility in rat soleus muscle: role of the Na+-K+ pump and Na+/K+ gradients (1999). https://pubmed.ncbi.nlm.nih.gov/10373703/ DOI: 10.1111/j.1469-7793.1999.0215r.x
    tissue_or_cell_type
    Soleus muscle

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 715–725

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated rat soleus, combined bath-ion perturbation. · source_derived_draft · unverified_draft

    ### k-na-gradients-muscle-excitability The combined 85 mM Na/9 mM K bath reduced M-wave area and tetanic force versus 147 mM Na/4 mM K. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Both sodium and potassium gradients matter for muscle activation. organism: Rat tissue_or_cell_type: Soleus muscle experimental_model: Isolated rat soleus, combined bath-ion perturbation. limitations: Combined perturbation cannot be attributed to potassium alone; not dietary excess. cross_nutrient: Reduced sodium and elevated potassium jointly impair excitability. [overgaard-1999-muscle] Relations between excitability and contractility in rat soleus muscle: role of the Na+-K+ pump and Na+/K+ gradients (1999). https://pubmed.ncbi.nlm.nih.gov/10373703/ DOI: 10.1111/j.1469-7793.1999.0215r.x
    Complete structured claim and evidence

In the sources

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