ENHANCED CA-45(2-MUSCLE CELLS FROM SPONTANEOUSLY HYPERTENSIVE RATS() EFFLUX IN CULTURED VASCULAR SMOOTH)

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-0(+)-dependent Ca2+ efflux), and the oth er is independent of extracellular sodium but is mediated by the Ca2pump (Na-0(+)- independent Ca2+ efflux). In the present study we have compared these two Ca2+ effluxes in cultured aortic smooth muscle cell s derived from spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY). In the presence of 100 nnol/L angiotensin II both Na+-Ca2+ exchange and Ca2+-pump-mediated Ca-45(2+) efflux were en hanced significantly in SHR compared to WKY. The cellular Ca-45 conten t was found to be increased in SHR compared to WKY. When the data were expressed as the fraction of Ca-45(2+) lost, defined as the ratio of Ca-45(2+) lost over each time interval (5 sec) to total cellular Ca-45 content during that period, Ca2+ efflux by both mechanisms was still higher in SHR. Our results suggest that the enhanced Ca-45(2+) efflux in response to angiotensin II in SHR may be linked to greater Ca2+ upt ake and possibly Ca2+ release from intracellular stores. An increase i n intracellular [Ca2+](i) may be compensated for by enhanced Ca2+-pump and Na+ Ca2+ exchange activities in VSMC in hypertension.