Alterations in calcium stores in aortic myocytes from spontaneously hypertensive rats

被引:46
作者
Cortes, SF [1 ]
Lemos, VS [1 ]
Stoclet, JC [1 ]
机构
[1] UNIV STRASBOURG 1, URA CNRS 600, LAB PHARMACOL & PHYSIOPATHOL CELLULAIRES, FAC PHARM, F-67041 ILLKIRCH GRAFFENSTADEN, FRANCE
关键词
ion transport; rats; inbred WKY; ryanodine; angiotensin II; intracellular; cell proliferation; spontaneously hypertensive;
D O I
10.1161/01.HYP.29.6.1322
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
The aim of the present work was to further characterize intracellular calcium stores released by angiotensin II (Ang II) in spontaneously hypertensive rat (SHR) and Wistar-Kyoto rat (WKY) vascular smooth muscle cells (VSMCs) and to study their alterations associated with proliferation. Intracellular Ca2+ concentration was monitored by image analysis in aortic myocytes loaded with fura 2. In the presence of extracellular Ca2+, sensitivity to Ang II in proliferating VSMCs was not different in the two strains, but it increased 10-fold in confluent VSMCs from SHR compared with those from WKY. In Ca2+-free medium, Ca2+ release induced by thapsigargin (10 mu mol/L) was significantly greater (about twofold) in SHR than WKY, in both proliferating and confluent cultures, with responses during proliferation being 0.7-fold smaller. Responses to Ang II were abolished after exposure of the cells to thapsigargin. In proliferating cultures, ryanodine (10 mu mol/L) did not modify the rises in intracellular Ca2+ concentration induced by Ang II in VSMCs from both strains. Conversely, in confluent cultures, ryanodine reduced Ang II (100 nmol/L)-induced Ca2+ release to the same level as in proliferating cultures, and it suppressed the difference between SHR and WKY. These results show that the ryanodine-sensitive Ca2+ release induced by Ang II is enhanced in VSMCs from SHR at confluence and is impaired during proliferation. Thus, they suggest that differences in Ca2+-induced Ca2+ release from the sarcoplasmic reticulum may participate in increased responsiveness of VSMCs to Ang II in SHR and in phenotypic modulation of vascular myocytes during proliferation.
引用
收藏
页码:1322 / 1328
页数:7
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