Wang Wen-Ze, Pang Li, Palade Philip
Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, 4301 W. Markham, Little Rock, AR 72205 USA.
Eur J Pharmacol. 2008 Dec 3;599(1-3):117-20. doi: 10.1016/j.ejphar.2008.09.034. Epub 2008 Sep 30.
Examination was made of the direct vascular effects of the hypertension-inducing pressor hormone angiotensin II on expression and activity of the voltage-gated calcium channel Ca(V)1.2. Freshly dissected rat superior mesenteric artery beds were maintained in organ culture unpressurized for 24 h in the presence or absence of angiotensin II. Relative to controls, angiotensin II increased Ca(V)1.2 protein expression and tension-inducing activity but not Ca(V)1.2 message. The increase in Ca(V)1.2 protein expression by angiotensin II was abrogated by damaging the endothelium. Thus, the endothelium is involved in regulating Ca(V)1.2 expression in the vascular wall.
研究了诱导高血压的升压激素血管紧张素II对电压门控钙通道Ca(V)1.2表达和活性的直接血管效应。将新鲜解剖的大鼠肠系膜上动脉床在有或无血管紧张素II的情况下于器官培养中在无压力状态下维持24小时。相对于对照组，血管紧张素II增加了Ca(V)1.2蛋白表达和张力诱导活性，但未增加Ca(V)1.2信使核糖核酸。血管紧张素II导致的Ca(V)1.2蛋白表达增加通过破坏内皮而被消除。因此，内皮参与调节血管壁中Ca(V)1.2的表达。
