Voltage-gated calcium channel and voltage-gated potassium channel (cardiac) (VGCC (for voltage-gated calcium channel), VGKC (for voltage-gated potassium channel))

Voltage-gated calcium and potassium channels are ion channels located in the cardiac cell membrane, which are critically involved in generating and shaping the cardiac action potential. Voltage-gated calcium channels (VGCCs), especially L-type (CaV1.2, CaV1.3) and T-type (CaV3.1), conduct Ca²⁺ into cardiac myocytes during depolarization, triggering excitation–contraction coupling and contributing to pacemaker activity and atrioventricular (AV) conduction[1][2][3][4][5]. Voltage-gated potassium channels (VGKCs) mediate K⁺ efflux, which is responsible for the repolarization phase of the cardiac action potential, restoring the resting membrane potential and determining action potential duration[6]. Dysfunctions of these channels, due to genetic mutations, acquired disease, or drug interactions, underlie many cardiac arrhythmias and conduction disorders. Both channel classes are established drug targets for antiarrhythmic and antihypertensive therapies.

Other names

Voltage-dependent calcium channelVoltage-gated K channelL-type calcium channel (CaV1.2, CaV1.3)T-type calcium channel (CaV3.1)KCNQ1hERG (for some VGKCs)CaVKV

Inhibition of Ca²⁺ influx to reduce cardiac contractility and conduction (for Ca channel blockers) - Inhibition of K⁺ efflux to prolong repolarization and action potential duration (for K channel blockers) - Suppression of abnormal automaticity or afterdepolarizations