Hilgers K F, Mann J F
Department of Medicine-Nephrology, University of Erlangen-Nuremberg, Fed. Rep. of Germany.
Arzneimittelforschung. 1993 Feb;43(2A):198-201.
Local vascular formation of angiotensin (Ang) peptides was investigated in isolated, plasma-free perfused rat hindquarters. Analysis of perfusate by high performance liquid chromatography and radioimmunoassay demonstrated spontaneous releases of Ang I and II from hindlimb vasculature. Captopril suppressed Ang II and increased Ang I levels. Formation of Ang peptides was abolished by bilateral nephrectomy but unaltered by subtotal 5/6 nephrectomy. Infused renin was taken up by hindlimb vasculature and led to substantial increases of local Ang formation and perfusion pressure. Both effects were sensitive to captopril (CAS 62571-86-2) and to the renin inhibitor H-142 (H-Pro-His-Pro-Phe-His-Leu-Val-Ile-His-OH). Conversion of Ang I to Ang II in hindquarter vasculature was approximately 75% and completely suppressed by captopril. Evidence for and against local vascular synthesis of renin is briefly discussed. In conclusion, the data indicate substantial local vascular formation of Ang I and II which, however, appears to be mainly due to plasma-derived renin.
在离体、无血浆灌注的大鼠后肢研究了血管紧张素(Ang)肽的局部血管生成情况。通过高效液相色谱法和放射免疫分析法对灌注液进行分析,结果表明后肢血管系统可自发释放Ang I和Ang II。卡托普利可抑制Ang II并提高Ang I水平。双侧肾切除可消除Ang肽的生成,但5/6肾次全切除对其无影响。注入的肾素被后肢血管系统摄取,导致局部Ang生成和灌注压力大幅增加。这两种效应均对卡托普利(CAS 62571-86-2)和肾素抑制剂H-142(H-脯氨酸-组氨酸-脯氨酸-苯丙氨酸-组氨酸-亮氨酸-缬氨酸-异亮氨酸-组氨酸-OH)敏感。后肢血管系统中Ang I向Ang II的转化率约为75%,且完全被卡托普利抑制。本文简要讨论了支持和反对肾素局部血管合成的证据。总之,数据表明Ang I和Ang II在局部血管大量生成,然而,这似乎主要归因于血浆来源的肾素。