Cardiac voltage-gated sodium and calcium channels (Nav/Cav channels)

Cardiac voltage-gated sodium and calcium channels are critical transmembrane proteins that orchestrate the electrical and mechanical activity of the heart. The primary sodium channel isoform, Nav1.5 (encoded by SCN5A), is responsible for the rapid influx of sodium ions that triggers the Phase 0 depolarization of the cardiac action potential, ensuring rapid impulse conduction (Source: PubMed 25324461). The predominant calcium channel, the L-type Cav1.2 (encoded by CACNA1C), mediates the influx of calcium ions during the plateau phase (Phase 2), which is essential for calcium-induced calcium release and subsequent myocardial contraction (Source: StatPearls NBK482430). Together, these channels define the shape and duration of the cardiac action potential and are fundamental to maintaining a rhythmic heartbeat. Dysfunctions in these channels, whether due to genetic mutations or drug interactions, are primary drivers of cardiac arrhythmias, heart failure, and sudden cardiac death (Source: PubMed 30595550). Therapeutic agents targeting these channels include Class I antiarrhythmics for sodium channels and Class IV antiarrhythmics or dihydropyridines for calcium channels, used to manage arrhythmias, hypertension, and angina (Source: PubChem).

Other names

Cardiac Na+ and Ca2+ channelsVoltage-gated sodium channel type V alpha subunit (Nav1.5)Voltage-dependent L-type calcium channel subunit alpha-1C (Cav1.2)SCN5A and CACNA1CCardiac voltage-dependent ion channels

Inhibition of ion conductance by binding to the alpha-subunit pore or stabilizing inactive channel conformations to modulate cardiac excitability and contractility.