摘要
肾素-血管紧张素系统(RAS)新成员的发现,改变了既往认为只有血管紧张素转化酶(ACE)催化生成的血管紧张素(Ang)Ⅱ才产生致病作用的观点,证明肾素与前肾素-肾素受体(RPR)的结合及AngⅣ与胰岛素调控氨基肽酶受体(IRAP)的结合同样也会产生致病作用。新发现的ACE2催化Ang-(1-7)和Ang-(1-9)的生成,Ang-(1-7)与Mas受体和Ang-(1-9)与AT2受体结合之后,可产生心血管保护作用,但RAS的致病作用仍然占优势。RAS新成员的发现,对认识RAS抑制剂的临床研究结果提供了新的理论依据。
The discovery of new members of renin-angiotensin system(RAS) changes the classical opinion that only angiotensin(Ang) Ⅱ converted by angiotensin-convertion enzyme(ACE) has a pathogenic role,besides renin binded renin-prorenin receptors(RPR) and Ang Ⅳ binded insulin-regulated amino peptidase receptors(IRAP).Ang-(1-7) and Ang-(1-9) are converted by newly finding ACE_2.Ang-(1-7) binding Mas receptors and Ang-(1-9) binding AT_2 receptors lead to cardiovascular protective effect.However,pathogenic role of RAS remains dominant.The discovery of new members of RAS supports new theoretical basis for recognition of the blockade of RAS in results of clinical trials.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2012年第2期83-87,共5页
Journal of Clinical Cardiology
基金
国家973课题资助项目(No:2007CB512005)