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《Chinese Journal of Arteriosclerosis》 2010-04
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Effects of AngiotensinⅡ on Adenosinetriphosphatases in Aortic Vascular Smooth Muscle Cells from Wistar-Kyoto Rats and Spontaneously Hypertensive Rats

ZHANG Gui-Hai,SHANG Qian-Hui,JIANG Qian-Fen,and WAN Wei-Hong (Institute of Clinical Medicine,Zunyi Medical College; Department of Cardiology,Affiliated Hospital of Zunyi Medical College,Zunyi,Guizhou 563003,China )  
Aim To explore the effects of angiotensinⅡon the activities of Ca2+-ATPase,Na+,K+-ATPase and mRNA expression levels of the plasma membrane Ca2+-ATPase isoform 1 (PMCA1) and Na+,K+-ATPase α1-subunit in cultured thoracic aortic vascular smooth muscle cells (ASMC) from Wistar-Kyoto rats and spontaneously hypertensive rats (SHR). Methods ASMC isolated from 14-week-old male Wistar-Kyoto rats and SHR were cultured,and treated with different concentrations (1×10-9,1×10-8,1×10-7 mol/L) of AngiotensinⅡ. The activities of Ca2+-ATPase,Na+,K+-ATPase were measured by biochemistry and enzymology. RT-PCR assay was employed to determine the relative levels of PMCA1 and Na+,K+-ATPase α1-subunit mRNA in ASMC. Results Low and moderate concentration (1×10-9,1×10-8 mol/L) of angiotensinⅡsignificantly increased the activity of Ca2+-ATPase in ASMC from Wistar-Kyoto rats(P0.05~P0.01),and the activity of Ca2+-ATPase was positively correlated with the intervention time of angiotensinⅡ( r=0.340,0.725),reached the maximum at 24 hours,up-regulated PMCA1 mRNA level at the same time (P0.05~P0.01); while high concentration (1×10-7 mol / L) angiotensinⅡ inhibited Ca2+-ATPase activity (P0.05),and the activity of Ca2 +-ATPase was negatively correlated with the intervention time(r=-0.348),reached the greatest effect at 24 hours,and simultaneously down-regulated PMCA1 mRNA level (P0.05). Angiotens inⅡ(1×10-9,1×10-8,1×10-7mol/L) decreased significantly the activity of Ca2 +-ATPase in ASMC from SHR (P0.05 ~P0.01),and the Ca2 +-ATPase activity was negatively correlated with the intervention time (r=-0.346,-0.493,-0.759),had the strongest effect at 24 hours,and simultaneously attenuated PMCA1 mRNA level. Three concentration of angiotensinⅡ (1×10-9,1×10-8,1×10-7mol/L) stimulated the activity of Na+,K+-ATPase in ASMC from Wistar-Kyoto rats in turn at24 hours,12 hours,6 hours (P0.05 ~P0.01),and increased the activity of Na+,K+-ATPase with α1-subunit mR-NA expression promoted in a dose-dependent manner at 24 hours (P0.05 ~P0.01),which was positively correlated with the intervention time of angiotens inⅡ(r=0.425,0.645,0.767 ). AngiotensinⅡ (1×10-9,1×10-8mol/L) didnot affect the activity of Na+,K+-ATPase in SHR (allP0.05),while angiotensinⅡ (1×10-7mol/L) significantly suppressed the activity of Na+,K+-ATPase,which was negatively correlated with the intervention time of angiotensinⅡ (r=-0.589),and reached maximum effect on the expression of Na+,K+-ATPaseα1-subunit mRNA at 24 hours (P0.05). Conclusion In Wistar-Kyoto rats,angiotens inⅡ has biphasic effects on Ca2 +-ATPase activity,PMCA1 mRNA expression,and activates Na+,K+-ATPase activity and α1 subunit mRNA expression in a dose-dependent manner in ASMC. Whereas,in SHR,angiotens inⅡ inhibits Ca2 +-ATPase activity and PMCA1 mRNA expression,and only highdose of angiotensinⅡ suppresses Na+,K+-ATPase activity andα1subunit mRNA expression in ASMC.
【Fund】: 贵州省科学技术基金重点项目;; 贵州省优秀科技教育人才省长专项资金[(2002)3013 (2005)239]
【CateGory Index】: R363
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【Citations】
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