Voltage-gated ion channels in cardiac myocytes (VGICs)

Voltage-gated ion channels in cardiac myocytes are specialized transmembrane proteins that open and close in response to changes in membrane potential, regulating the selective flow of sodium, potassium, and calcium ions (StatPearls, NBK526062). These channels are the fundamental drivers of the cardiac action potential, which coordinates the rhythmic contraction and relaxation of the heart chambers (PubMed, PMC4124750). Key members of this group include the voltage-gated sodium channel (Nav1.5), L-type calcium channels (Cav1.2), and various potassium channels such as the rapid delayed rectifier (hERG) (UniProt, P35498). Dysfunction in these channels, resulting from genetic mutations or structural heart disease, leads to various arrhythmias and sudden cardiac death (NIH, GeneReviews). Pharmacological modulation of these channels is a primary strategy for treating arrhythmias, although such interventions require careful monitoring due to the inherent risk of proarrhythmia and adverse effects on cardiac conduction (PubMed, PMC2883916).

Other names

Cardiac voltage-gated ion channelsCardiac ion channelsVoltage-dependent ion channels of the heart

Drugs targeting these channels typically act as pore blockers or gating modifiers that inhibit the flux of specific ions (Na+, K+, or Ca2+) across the sarcolemma, thereby altering the depolarization, plateau, or repolarization phases of the cardiac action potential to suppress abnormal electrical activity (StatPearls, NBK526062).