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L-type calcium channel protein CaV1.2 in vascular smooth muscle cells is the principal calcium channel controlling calcium influx, which is essential for myogenic tone, contractility, transcriptional regulation, and vascular reactivity. CaV1.2 channels are high-voltage activated, composed of pore-forming α1c and auxiliary subunits, and subject to regulation by phosphorylation, auxiliary proteins, and signaling molecules. Their altered activity is implicated in diseases like hypertension and diabetes. Pharmacological blockade of these channels with calcium channel blockers (CCBs, including dihydropyridines and non-dihydropyridines) is a key strategy for treating cardiovascular diseases such as hypertension and angina, though challenges regarding selectivity and adverse effects still persist[1][5][6][7].
Inhibition or blockade of L-type calcium channels, reducing calcium influx\nLowering intracellular calcium concentration, promoting vasodilation, and reducing vascular tone[5][7]\nDecreased arterial resistance, reduction in blood pressure\nReduced oxygen demand, antianginal effects
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