血管紧张素Ⅱ引起血管平滑肌细胞内Ca^(2+)浓度变化机制的研究  

Mechanism of Cytosolic Ca^(2+) Concentration Changes Caused by AngiotensinⅡ in Vascular Smooth Muscle Cells

作　　者：周莹[1] 刘沛[1] 

机构地区：[1]中国医科大学附属第一医院传染科,沈阳110001

出　　处：《中国医科大学学报》2008年第3期299-301,共3页Journal of China Medical University

基　　金：国家自然科学基金资助项目(30170849)

摘　　要：目的探讨血管紧张素Ⅱ(AngⅡ)调节血管平滑肌细胞(VSMC)内游离钙离子浓度([Ca2+]i)的作用机制。方法应用改进的组织块贴壁法分离培养大鼠主动脉VSMC。采用Fluo-3/AM负载,应用confocal显微镜观察VSMC内[Ca2+]i的变化。实验分为对照组和三磷酸肌醇受体系统(IP3Rs)阻断剂2-APB组。结果胞外无钙的情况下AngⅡ可引起一个快速、明显的[Ca2+]i升高,而2-APB组[Ca2+]i仅轻度升高,与对照组比较有显著差异(P<0.05)。结论AngⅡ与其受体AT1结合,激活IP3RS系统促进细胞内储备钙释放,调节VSMC内[Ca2+]i变化。Objective To investigate the mechanism of the changes in cytosohc [Ca^2＋]i caused by angiotensin Ⅱ （Ang Ⅱ ） in vascular smooth muscle cells （VSMC）. Melhods The cytosolic [Ca^2＋]i in Fluo-3/AM loaded VSMC was determined by confocal microscope. Rat VSMCs were isolated from aortic explants. There were control and 2-APB （inhibitor of inositol-1,4,5-trisphosphate receptor system（IP3Rs） ） groups in our experiment. Results There was a rapid, obvious increase of [ Ca^2＋ ]i caused by Ang Ⅱ in the control group, but no obvious increase in 2-APB blocking group （ 13.09±9.83 vs gl 1.64±80.27 nmol/L, P 〈 0.05）. Condusion The main mechanism of Ang Ⅱ -induced [Ca^2＋]i changes in VSMC is that Ang Ⅱ combined with AT1 receptor,activates IP3Rs and stimulate cytisolic reserved calcium to release.

关 键 词：血管紧张素Ⅱ 胞内游离钙离子浓度 三磷酸肌醇受体 

分 类 号：R331.3[医药卫生—人体生理学]