Vascular smooth muscle cell calcium entry mechanisms

Vascular smooth muscle cell (VSMC) calcium entry mechanisms encompass the various pathways through which extracellular calcium ions enter the cytoplasm to trigger contraction and regulate cellular signaling (PMID: 29133221). The primary pathway is via voltage-gated L-type calcium channels (e.g., Cav1.2), which open in response to membrane depolarization to initiate the contractile apparatus (PMID: 25172231). Other significant mechanisms include store-operated calcium entry (SOCE) mediated by STIM and Orai proteins, receptor-operated calcium channels (ROCCs) often involving the Transient Receptor Potential (TRP) channel family, and T-type calcium channels (PMID: 28213295). These mechanisms are critical for maintaining vascular tone and blood pressure; their dysregulation is linked to cardiovascular diseases such as hypertension, vasospasm, and atherosclerosis (PMID: 30104244). Pharmacological targeting of these pathways, most notably with L-type calcium channel blockers (CCBs) like amlodipine, is a cornerstone of antihypertensive therapy, promoting vasodilation by reducing the availability of calcium for myosin light chain phosphorylation (StatPearls: NBK482474).

Other names

VSMC calcium influxVascular calcium entry pathwaysCalcium signaling in vascular smooth muscle

Inhibition of calcium influx through voltage-gated or receptor-operated channels to reduce intracellular calcium levels and promote vasodilation.