Intracellular alkalinization augments capacitative Ca2+ entry in vascular smooth muscle cells

Agonist-induced Ca2+ influx of vascular smooth muscle cells is thought to be triggered by depletion of intracellular Ca2+ stores. This study investigated the effects of intracellular alkalinization on capacitative Ca2+ entry in A7r5 rat aortic smooth muscle cells. Intracellular alkalinization was induced by NH(4)Cl. Transplasmalemmal Ca2+ influx due to Ca2+ 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 NH(4)Cl. Neither 5-hydroxytryptamine-induced inositol monophosphate accumulation nor intracellular Ca2+ release from its stores was affected by NH(4)Cl. These results suggest that intracellular alkalinization acts on the process(es) after depletion of Ca2+ stores and facilitates capacitative Ca2+ entry in vascular smooth muscle cells.