Intracellular Ca2+ release in cerebral arteries

Vasoconstricting agonists elevate the intracellular Ca2+ concentration and induce tension development in vascular smooth muscle cells by inducing both Ca2+ influx from the extracellular space and Ca2+ release from cellular stores. The relative importance of Ca2+ release has been found to vary between different sites in the vasculature. This review examines the role of Ca2+ release in the activation of cerebral arteries produced by several vasoconstricting stimuli. Although the activation of cerebral arteries by agonists such as 5-hydroxytryptamine and noradrenaline has typically been found to have little dependence on Ca2+ release, other vasoconstrictors such as thromboxane A2, which may be released from the endothelium by other agonists, appear to induce a substantial intracellular Ca2+ release in cerebral arteries. The limited efficacy of Ca2+ influx blockers in the treatment of delayed cerebrovascular constriction occurring as a result of subarachnoid haemorrhage suggests that intracellular mechanisms such as Ca2+ release and/or the activation of protein kinase C may be important determinants of vasoconstriction under pathological conditions.