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

Voltage-dependent calcium channels (VDCCs) in smooth muscle cells, primarily the L-type (Cav1.2) isoform, are critical regulators of muscle tone and vascular resistance [3, 7]. These channels open in response to membrane depolarization, allowing an influx of extracellular calcium ions that triggers the contraction of smooth muscle through the activation of calmodulin and myosin light-chain kinase [8, 10]. In the vasculature, this process is essential for maintaining blood pressure and regulating blood flow to various organs [17]. Dysregulation of these channels is a key factor in the pathogenesis of hypertension and vasospastic disorders [16]. Consequently, they are the primary targets for calcium channel blockers (CCBs), which are widely used to treat cardiovascular conditions by inducing vasodilation and reducing systemic vascular resistance [4, 15]. These drugs are categorized into dihydropyridines, which are selective for vascular smooth muscle, and non-dihydropyridines, which also affect cardiac conduction and contractility [14].

Other names

CACNA1CCav1.2L-type voltage-gated calcium channelVoltage-dependent L-type calcium channelDHP-sensitive calcium channelCalcium channel, voltage-dependent, L type, alpha 1C subunit

Inhibition of calcium ion influx through the L-type voltage-gated calcium channel pore, leading to a decrease in intracellular calcium concentration and subsequent relaxation of smooth muscle cells (vasodilation) [4, 14].