INTRACELLULAR CA2-ARTERIES( RELEASE IN CEREBRAL)

Vasoconstricting agonists elevate the intracellular Ca2+ concentration and induce tension development in vascular smooth muscle cells by ind ucing both Ca2+ influx from the extracellular space and Ca2+ release f rom 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 arteri es produced by several vasoconstricting stimuli. Although the activati on of cerebral arteries by agonists such as 5-hydroxytryptamine and no radrenaline has typically been found to have little dependence on Ca2 release, other vasoconstrictors such as thromboxane A(2), which may b e released from the endothelium by other agonists, appear to induce a substantial intracellular Ca2+ release in cerebral arteries. The limit ed efficacy of Ca2+ influx blockers in the treatment of delayed cerebr ovascular constriction occurring as a result of subarachnoid haemorrha ge suggests that intracellular mechanisms such as Ca2+ release and/or the activation of protein kinase C may be important determinants of va soconstriction under pathological conditions.