Enhanced 45Ca2+ efflux in cultured vascular smooth muscle cells from spontaneously hypertensive rats.

Ca2+ efflux from cultured vascular smooth muscle cells (VSMC) consists of two mechanisms: one is dependent on extracellular sodium, mediated by the Na(+)-Ca2+ exchange (Na+o-dependent Ca2+ efflux), and the other is independent of extracellular sodium but is mediated by the Ca(2+)-pump (Na+o-independent Ca2+ efflux). In the present study we have compared these two Ca2+ effluxes in cultured aortic smooth muscle cells derived from spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY). In the presence of 100 nmol/L angiotensin II both Na(+)-Ca2+ exchange and Ca(2+)-pump-mediated 45Ca2+ efflux were enhanced significantly in SHR compared to WKY. The cellular 45Ca content was found to be increased in SHR compared to WKY. When the data were expressed as the fraction of 45Ca2+ lost, defined as the ratio of 45Ca2+ lost over each time interval (5 sec) to total cellular 45Ca content during that period, Ca2+ efflux by both mechanisms was still higher in SHR. Our results suggest that the enhanced 45Ca2+ efflux in response to angiotensin II in SHR may be linked to greater Ca2+ uptake and possibly Ca2+ release from intracellular stores. An increase in intracellular [Ca2+]i may be compensated for by enhanced Ca(2+)-pump and Na(+)-Ca2+ exchange activities in VSMC in hypertension.