Intracellular Alkalinization Augments Capacitative Ca2+ Entry in Vascular Smooth Muscle Cells

Agonist-induced Ca influx of vascular smooth muscle cells is thought to be triggered by depletion of intracellular Ca stores. This study investigated the effects of intracellular alkalinization on capacitative Ca entry in A7r5 rat aortic smooth muscle cells. Intracellular alkalinization was induced by NH4Cl. Transplasmalemmal Ca influx due to Ca store depletion induced by thapsigargin, which was abolished by pretreatment of the cells with SKF-96365 but not affected by that with verapamil, was significantly increased by pretreatment with NH4Cl. Neither 5-hydroxytryptamine-induced inositol monophosphate accumulation nor intracellular Ca release from its stores was affected by NH4Cl. These results suggest that intracellular alkalinization acts on the process(es) after depletion of Ca stores and facilitates capacitative Ca entry in vascular smooth muscle cells.