Vascular smooth muscle intracellular calcium handling

Vascular smooth muscle intracellular calcium handling is the integrated physiological system responsible for regulating cytosolic calcium concentrations ([Ca2+]i) to modulate vascular tone and blood pressure. This process involves the influx of extracellular calcium through L-type voltage-gated calcium channels (VGCCs) and store-operated channels, as well as the release of calcium from the sarcoplasmic reticulum (SR) via inositol trisphosphate receptors (IP3R) and ryanodine receptors (RyR) [1][2]. To maintain homeostasis and induce relaxation, calcium is removed from the cytoplasm by the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) pump, the plasma membrane Ca2+-ATPase (PMCA), and the sodium-calcium exchanger (NCX) [3]. Dysregulation of these handling mechanisms, such as increased channel activity or impaired sequestration, is a primary driver of hypertension, vasospasm, and atherosclerosis [1][3]. Therapeutic strategies targeting this system include calcium channel blockers (CCBs), which directly inhibit influx, and vasodilators that enhance calcium removal pathways to reduce peripheral resistance [4].

Other names

VSMC calcium signalingVascular smooth muscle calcium homeostasisExcitation-contraction coupling in vascular smooth muscleCalcium handling in vascular smooth muscle

Pharmacological agents typically act by inhibiting L-type voltage-gated calcium channels to reduce extracellular influx, or by stimulating the production of cyclic nucleotides (cAMP/cGMP) which activate protein kinases that promote calcium sequestration into the sarcoplasmic reticulum via SERCA and extrusion via PMCA [1][2][4].