Voltage-dependent L-type calcium channel subunit alpha-1C (CACNA1C) (Cav1.2)

Voltage-dependent L-type calcium channel subunit alpha-1C, commonly known as Cav1.2, is a pore-forming protein essential for calcium ion influx in response to membrane depolarization. It is highly expressed in the myocardium and vascular smooth muscle, where it serves as the primary mediator of excitation-contraction coupling (UniProt: Q13936). In cardiac myocytes, Cav1.2 activity sustains the action potential plateau and triggers the release of internal calcium stores, facilitating heart contraction (NCBI Gene: 775). In vascular smooth muscle, it regulates arterial tone, thereby influencing systemic blood pressure and peripheral resistance. Dysregulation or mutations in Cav1.2 are linked to cardiovascular diseases such as hypertension, Brugada syndrome, and Timothy syndrome (PubMed: 25135136). Consequently, Cav1.2 is a major therapeutic target for calcium channel blockers like amlodipine and verapamil, which are used to manage hypertension and angina by promoting vasodilation and reducing myocardial oxygen demand (StatPearls: NBK482473).

Other names

CACNA1CCalcium channel voltage-dependent L type alpha 1C subunitCCHL1A1CaV1.2L-type voltage-gated calcium channel alpha 1C subunit

Antagonism of the L-type calcium channel to inhibit calcium influx into excitable cells, resulting in vascular smooth muscle relaxation (vasodilation) and decreased myocardial contractility and conduction velocity.