血管紧张素Ⅱ对血管平滑肌细胞血管紧张素Ⅱ受体1、2mRNA表达的影响  

Differential expression of AT1R and AT2R mRNA in vascular smooth muscle cells induced by AngⅡ

作　　者：魏钧伯[1] 马健[1] 陆志刚[1] 马士新[1] 赵钢[1] 蔡迺绳[2] 魏盟[1] 

机构地区：[1]上海市第六人民医院心内科,上海200233 [2]复旦大学附属中山医院心内科

出　　处：《临床心血管病杂志》2015年第2期216-217,共2页Journal of Clinical Cardiology

摘　　要：目的:观察血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)对血管平滑肌细胞(VSMC)血管紧张素Ⅱ受体1(AT1R)、血管紧张素Ⅱ受体2(AT2R)mRNA表达的影响。方法:人脐带动脉平滑肌细胞体外原代培养,AngⅡ干预后RT-PCR测定VSMC的AT1R、AT2R mRNA的表达,并观察AT1R阻滞剂氯沙坦、AT2R阻滞剂PD123319对AngⅡ上述诱导作用的影响。结果:1AngⅡ作用于VSMC后,AT1R mRNA表达增强(P<0.01),氯沙坦阻断AT1R后,AT1R mRNA表达显著下降(P<0.01),PD123319阻断AT2R后,AT1R mRNA表达无显著性变化;2AngⅡ作用于VSMC后,AT2R mRNA表达无显著性增强,氯沙坦及PD123319作用后,AT2R mRNA表达也未见显著性变化。结论:1AngⅡ可诱导VSMC AT1R mRNA表达,AT1R在此过程中起重要介导作用,AT1R阻滞剂氯沙坦可有效抑制AngⅡ的这种诱导作用;2相对于AT1R,AngⅡ不能诱导VSMC AT2R mRNA表达增加。所以推测AngⅡ差异化诱导VSMC AT1R、AT2R mRNA表达,导致AT1R、AT2R失衡。Objective ：To detect the impacts of angiotensinⅡ （AngⅡ ） on ATIR and AT2R mRNA expression in vascular smooth muscle ceils （VSMC）. Method： Smooth muscle cells of human umbilical artery were isolated and cultured in vitro. Then, the mRNA expressions of VSMC ATIR＇ and AT2R after interaction with Ang Ⅱ were detected. Furthermore, the impact of Losartan（AT1R） and PD123319（AT2R） on the above effects of Ang Ⅱ was observed. Result： ① The expression of VSMC ATIR mRNA was increased after stimulated with Ang Ⅱ （P〈 0. 01）, but depressed significantly by Losartan （P〈0.01）. There was no obvious change of AT1R mRNA expression after AT2R blocked by PD123319. ②No change of AT2R mRNA expression was found after induced by Ang , which also observed after co-incubation with Losartan or PD123319 with Losartan or PD123319. Conclusion： ①Ang Ⅱ increases the expression of VSMC AT1R mRNA, which can be blocked by Losartan. ②Ang Ⅱ can ＂t increase mRNA expression of AT2R. The different effects of Ang Ⅱ might lead to the unbalance of AT1R and AT2R.

关 键 词：动脉粥样硬化 血管紧张素Ⅱ 血管紧张素Ⅱ受体 

分 类 号：R541.4[医药卫生—心血管疾病]