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- W2116798614 abstract "Voltage-gated sodium (NaV) channels generate the upstroke and mediate duration of the ventricular action potential, thus they play a critical role in mediating cardiac excitability. Cardiac ischemia triggers extracellular pH to drop as low as pH 6.0, within just 10 min of its onset. Heightened proton concentrations reduce sodium conductance and alter the gating parameters of the cardiac-specific voltage-gated sodium channel, NaV1.5. Most notably, acidosis destabilizes fast inactivation, which plays a critical role in regulating action potential duration. The changes in NaV1.5 channel gating contribute to cardiac dysfunction during ischemia that can cause syncope, cardiac arrhythmia, and even sudden cardiac death. Understanding NaV channel modulation by protons is paramount to treatment and prevention of the deleterious effects of cardiac ischemia and other triggers of cardiac acidosis." @default.
- W2116798614 created "2016-06-24" @default.
- W2116798614 creator A5017211526 @default.
- W2116798614 creator A5035075884 @default.
- W2116798614 date "2014-01-01" @default.
- W2116798614 modified "2023-09-27" @default.
- W2116798614 title "Proton Modulation of Cardiac I Na: A Potential Arrhythmogenic Trigger" @default.
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- W2116798614 doi "https://doi.org/10.1007/978-3-642-41588-3_8" @default.
- W2116798614 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24737236" @default.
- W2116798614 hasPublicationYear "2014" @default.
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