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

被引：13

作者：

CHEN, S ^{[1
]}

ROUFOGALIS, BD ^{[1
]}

机构：

[1] UNIV SYDNEY,DEPT PHARM,SYDNEY,NSW 2006,AUSTRALIA

来源：

AMERICAN JOURNAL OF HYPERTENSION | 1994年 / 7卷 / 07期

关键词：

SPONTANEOUSLY HYPERTENSIVE RAT; SMOOTH MUSCLE CELLS; CA2+ PUMP EFFLUX; NA+-CA2+ EXCHANGE; ANGIOTENSIN II;

D O I：

10.1093/ajh/7.7.597

中图分类号：

R6 [外科学];

学科分类号：

1002 ; 100210 ;

摘要：

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 other is independent of extracellular sodium but is mediated by the Ca2+ pump (Na-0(+)- 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 nnol/L angiotensin II both Na+-Ca2+ exchange and Ca2+-pump-mediated Ca-45(2+) efflux were enhanced significantly in SHR compared to WKY. The cellular Ca-45 content 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+ uptake and possibly Ca2+ release from intracellular stores. An increase in intracellular [Ca2+](i) may be compensated for by enhanced Ca2+-pump and Na+ Ca2+ exchange activities in VSMC in hypertension.

引用

页码：597 / 602

页数：6

共 34 条

[1] Dominiczak A.F., Bohr D.F., Cell membrane abnormalities and regulation of intracellular calcium concentration in hypertension, Clin Sei, 79, pp. 415-423, (1990)
[2] Bendhack L.M., Sharma R.V., Bhalla R.C., Altered signal transduction in vascular smooth muscle cells of spontaneously hypertensive rats, Hypertension, 19, pp. 11-142, (1992)
[3] Sugiyama T., Yoshizumi M., Takaku F., Et al., Abnormal calcium handling in vascular smooth muscle cells of spontaneously hypertensive rats, J Hypertens, 8, pp. 369-375, (1990)
[4] Sugiyama T., Yoshizumi M., Takaku F., Et al., The elevation of the cytosolic calcium ions in vascular smooth muscle cells in SHR: Measurement of the free calcium ions in single living cells by laser microflurospectrom-etry, Biochem Biophys Res Commun, 141, pp. 340-345, (1986)
[5] Bukoski R.D., Intracellular Ca2+ metabolism of isolated resistance arteries and cultured vascular myocytes of spontaneously hypertensive and Wistar-Kyoto nor-motensive rats, J Hypertens, 8, pp. 37-43, (1990)
[6] Robinson B.F., Altered calcium handling as a cause of primary hypertension, J Hypertens, 2, pp. 1-6, (1984)
[7] Furukawa K.-I., Tawada Y., Shigekawa M., Regulation of the plasma membrane Ca2+ pump by cyclic nucleotides in cultured vascular smooth muscle cells, J Biol Chem, 263, pp. 8058-8065, (1988)
[8] Smith J.B., Zheng T., Smith L., Relationship between cytosolic free calcium and Na + -Ca2+ exchange in aortic muscle cells, Am J Physiol, 256, pp. C147-C154, (1989)
[9] Cauvin C., John A., Yamamoto H., Et al., Ca2+ movements in vascular smooth muscle and their alterations in hypertension, Membrane Abnormalities in Hypertension, pp. 145-179, (1989)
[10] Orlov S., Resink T.J., Bernhardt J., Et al., Vascular smooth muscle cell calcium fluxes: Regulation by angiotensin II and lipoproteins, Hypertension, 21, pp. 195-203, (1993)

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