摘要
血管紧张素Ⅱ(AngⅡ)是肾素-血管紧张素系统中最主要的活性物质,与受体结合后可激活蛋白激酶C(PKC),活化的PKC可以通过各种信号转导途径,促进心肌成纤维细胞增殖,诱导心肌纤维化,导致心室重构。血管紧张素Ⅱ受体(AT1受体)拮抗剂,可以阻滞AngⅡ促心血管细胞增殖肥大作用,同时AT1受体被阻断后,反馈性地使血浆肾素增加2～3倍,导致血浆中的AngⅡ浓度升高。由于AT1受体已经被阻滞,这些反馈作用难以表现。但血浆中升高的AngⅡ通过激活AT2受体,进而激活缓激肽-一氧化氮途径,产生舒张血管、降低血压、抑制心血管重构等作用。
Angiotensin Ⅱ（AngⅡ） is the primary active substance in renin-angiotensin system.The binding of AngⅡ to its receptor activates protein kinase C（PKC）,which promote myocardial fibroblast proliferation,induce myocardial fibrosis,and results in ventricular remodelling through a variety of signaling pathways.AngⅡ receptor（AT1 receptor） antagonist interrupt the proliferative and hypertrophic effects of AngⅡ on cardiovascular cells.The blockage of AT1 receptor increases serum renin by 2-3 times in a feedback manner and raises plasma AngⅡ concentration.However,such feedbacks are not clinically significantly due to the blockage of AT1 receptor.The increased plasma AngⅡ activates AT2 receptor and further bradykinin-NO pathway to be effective in vasodilation,antihypertension and inhibition of cardiovascular remodelling.
出处
《医学综述》
2011年第6期867-869,共3页
Medical Recapitulate
