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The **Voltage-dependent L-type calcium channel alpha-1C subunit** (CaV1.2, encoded by the CACNA1C gene) is the main pore-forming subunit of L-type voltage-gated calcium channels. It mediates the entry of calcium ions into cells upon membrane depolarization, a process that is crucial in cardiac and smooth muscle contraction, neuronal signaling, and various forms of signal transduction. CaV1.2 channels play an essential role in excitation-contraction coupling in the heart, helping shape the cardiac action potential and enabling calcium-induced calcium release from intracellular stores. These channels are the primary targets of the dihydropyridine class of calcium channel blockers, which are widely used to treat hypertension, angina, and arrhythmias. Mutations in the CACNA1C gene are associated with a variety of cardiovascular and neuropsychiatric diseases[1][3][7][8].
Blockade of L-type calcium channel (inhibits calcium influx); Decreases cardiac contractility; Vasodilation via smooth muscle relaxation; Reduction in heart rate (negative chronotropy); Antiarrhythmic effect
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