Abstract
Contraction of vascular smooth muscle cells (VSMCs) depends on the rise of cytosolic [Ca 2+] owing to either Ca 2+ influx through voltage-gated Ca 2+ channels of the plasmalemma or to receptor-mediated Ca 2+ release from the sarcoplasmic reticulum (SR). Although the ionotropic role of L-type Ca 2+ channels is well known, we review here data suggesting a new role of these channels in arterial myocytes. After sensing membrane depolarization Ca 2+ channels activate G proteins and the phospholipase C/inositol 1,4,5-trisphosphate (InsP 3) pathway. Ca 2+ released through InsP 3-dependent channels of the SR activates ryanodine receptors to amplify the cytosolic Ca 2+ signal, thus triggering arterial cerebral vasoconstriction in the absence of extracellular calcium influx. This metabotropic action of L-type Ca 2+ channels, denoted as calcium channel-induced Ca 2+ release, could have implications in cerebral vascular pharmacology and pathophysiology, because it can be suppressed by Ca 2+ channel antagonists and potentiated with small concentrations of extracellular vasoactive agents as ATP.
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