Objective: To determine whether vasculature depends on circulatory or locally produced renin toinitiate its renin angiotensin-aldosterone system (RAAS), and to evaluate the effect of nephrectomy on vascular aldosterone biosynthesis. Methods: The expression of vascular renin mRNA was observed by reversetranscription polyrnerase chain reaction (RT-PCR) 30 h after nephrectomy, and the production of aldosteroneand angiotensin Ⅱ in vessels measured by high performance liquid chromatography (HPLC) and radioimmunoassay (RIA). Results: Aorta was still able to express renin mRNA after nephrectorny when plasmarenin activity disappeared. There were no significant differences among the control group, the sham operationgroup and the nephrectomy group for both the levels of aldosterone and angiotensin Ⅱ (P >0. 05) althoughthe levels of both ACTH and potassium were significantly increased in the nephrectomy group as comparedwith the control group (P <0. 01 ). However, there were significant differences between the control groupand ACEI-perindopril group for both aldosterone and angiotensin Ⅱ (P <0. 05). Conclusion: The resultssuggest that there exists an independent RAAS in vasculature which is different from that of the heart whichdepends on plasma renin and the biosynthesis of vascular aldosterone is induced mainly by angiotensin Ⅱ.
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