Voltage-dependent L-type calcium channel subunit alpha-1C [1, 2, 3, 7] (Cav1.2 [1, 3, 4, 6, 7])

The L-type calcium channel Cav1.2, primarily composed of the pore-forming alpha-1C subunit (encoded by the CACNA1C gene), is a critical voltage-gated ion channel found in cardiac and vascular smooth muscle cells [1, 2, 3, 7]. In vascular smooth muscle, Cav1.2 mediates the influx of calcium ions in response to membrane depolarization, which is the fundamental trigger for muscle contraction and the maintenance of myogenic tone [7, 8, 11, 14, 15]. This process is essential for the regulation of peripheral vascular resistance and systemic blood pressure [7, 11]. Dysregulation or overactivity of Cav1.2 is a central factor in the pathogenesis of hypertension, while mutations in the CACNA1C gene are linked to severe conditions like Timothy syndrome and cardiac arrhythmias [2, 3, 5, 8, 10]. Consequently, Cav1.2 is a major therapeutic target for a wide range of cardiovascular drugs, most notably the dihydropyridine, phenylalkylamine, and benzothiazepine classes of calcium channel blockers [6, 8, 9, 13]. These drugs act as antagonists that inhibit calcium entry, leading to vasodilation and reduced cardiac workload, making them first-line treatments for hypertension and angina [8, 9, 10].

Other names

CACNA1C [1, 3, 4]CACH2 [1, 3, 4]CACN2 [1, 3, 4]CACNL1A1 [1, 3, 4]CCHL1A1 [1, 3, 4]LQT8 [1, 3, 4]TS [1, 3, 4]Calcium voltage-gated channel subunit alpha1 C [1, 2, 3]Voltage-gated calcium channel subunit alpha Cav1.2 [3, 7]

Antagonist of the L-type calcium channel, inhibiting calcium ion influx into smooth muscle and cardiac cells [8, 9, 10].