Chen S, Roufogalis B D
Department of Pharmacy, University of Sydney, New South Wales, Australia.
Am J Hypertens. 1994 Jul;7(7 Pt 1):597-602. doi: 10.1093/ajh/7.7.597.
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.
培养的血管平滑肌细胞（VSMC）中的Ca2+外流由两种机制组成：一种依赖细胞外钠，由钠钙交换介导（钠依赖型Ca2+外流），另一种不依赖细胞外钠，但由钙泵介导（钠非依赖型Ca2+外流）。在本研究中，我们比较了源自自发性高血压大鼠（SHR）和Wistar-Kyoto正常血压大鼠（WKY）的培养主动脉平滑肌细胞中的这两种Ca2+外流。与WKY相比，在存在100 nmol/L血管紧张素II的情况下，SHR中钠钙交换和钙泵介导的45Ca2+外流均显著增强。发现SHR中的细胞45Ca含量比WKY增加。当数据表示为45Ca2+丢失的分数时，定义为每个时间间隔（5秒）内丢失的45Ca2+与该时间段内细胞总钙含量的比率，SHR中两种机制的Ca2+外流仍然更高。我们的结果表明，SHR中对血管紧张素II反应增强的45Ca2+外流可能与更多的Ca2+摄取以及可能从细胞内储存释放的Ca2+有关。高血压中VSMC中细胞内[Ca2+]i的增加可能通过增强钙泵和钠钙交换活性来补偿。
