组织中肾素-血管紧张素-醛固酮系统的实验研究  

AN EXPERIMENTAL STUDY ON TISSUE RENIN ANGIOTENSIN ALDOSTERONE SYSTEM

作　　者：吴平生[1] 梁欣伟[1] 郭志刚[1] 聂道海 张远慧[1] 刘伊丽[1] 

机构地区：[1]第一军医大学南方医院心内科

出　　处：《中华内科杂志》1997年第9期591-594,共4页Chinese Journal of Internal Medicine

基　　金：广东省自然科学基金

摘　　要：为了解组织中肾素－血管紧张素－醛固酮系统情况，用离体肾灌注、高效液相分析、放免检测、肾素基因保留时间（ＲＴ）－ＰＣＲ检测首次证明肾脏也可合成醛固酮。双肾切除３０小时使血浆肾素活性消失之后，用ＲＴ－ＰＣＲ技术表明血管仍可表达肾素ｍＲＮＡ，从而说明血管不同于心脏、具有独立的肾素合成能力。血管紧张素转换酶抑制剂培哚普利，不仅可抑制血管局部血管紧张素Ⅱ的生成，还可抑制血管醛固酮的合成，从而进一步解释培哚普利逆转血管重构的作用机理。Aldosterone biosynthesis in kidney has been proved by means of kidney perfusion in vitro, high performance liquid chromatography, radioimmunoassay and RT PCR, indicating that aldosterone biosynthesis is possible in tissues other than adrenal. Bilateral nephrectomy was carried out in male Wistar rats and the plasma renin activity would disappear after 30 hours. However, RT PCR showed that the vasculature in the nephrectomized rats was still able to express renin mRNA. It means that the vasculature is different from the heart which depends on taking up renin from the circulation, while the vasculature takes renin produced locally in its own tissue to initiate the renin angiotensin aldosterone system. Perindopril, an angiotensin converting enzyme inhibitor (ACEI), inhibits not only the production of angiotensin Ⅱ, but also the synthesis of aldosterone in the vasculature. ACEI reversion of vascular remodeling is probably related with its inhibition of aldosterone synthesis in the vasculature.

关 键 词：组织学 肾素 血管紧张素系统 高血压 降压药 

分 类 号：R544.105[医药卫生—心血管疾病] R972.4[医药卫生—内科学]