Perich R, Jackson B, Paxton D, Johnston C I
Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australia.
J Hypertens. 1992 Feb;10(2):149-53. doi: 10.1097/00004872-199202000-00007.
Abnormalities in the vascular renin-angiotensin system have been hypothesized to contribute to the pathogenesis and complications of hypertension. In animal models of hypertension, there is wide variation in reported vascular angiotensin converting activity, particularly in cerebral microvessels. In this study, we sought to characterize, quantitate and compare cerebral microvessel angiotensin converting enzyme (ACE) in genetically hypertensive rats and normotensive rats.
Brain microvascular ACE from 14-week-old spontaneously hypertensive rats (SHR) was measured and compared with ACE from brain microvessels of normotensive Wistar-Kyoto (WKY) controls.
Isolated cerebral microvascular ACE was measured using two methods, enzyme kinetic assay or radioligand binding assay.
In SHR, cerebral microvessel ACE was of similar activity and concentration and had similar ligand binding affinities to WKY rats. Plasma ACE activity was significantly elevated in WKY rats compared with SHR.
Cerebral microvascular ACE is similar in SHR and WKY rats. Microvascular ACE is unlikely to participate in the pathogenesis or complications of hypertension in this model.
血管肾素 - 血管紧张素系统异常被认为与高血压的发病机制及并发症有关。在高血压动物模型中,所报道的血管血管紧张素转换活性存在很大差异,尤其是在脑微血管中。在本研究中,我们试图对遗传性高血压大鼠和正常血压大鼠的脑微血管血管紧张素转换酶(ACE)进行表征、定量并比较。
测量14周龄自发性高血压大鼠(SHR)脑微血管ACE,并与正常血压的Wistar - Kyoto(WKY)对照大鼠脑微血管中的ACE进行比较。
使用酶动力学测定法或放射性配体结合测定法测量分离的脑微血管ACE。
在SHR中,脑微血管ACE的活性、浓度及配体结合亲和力与WKY大鼠相似。与SHR相比,WKY大鼠的血浆ACE活性显著升高。
SHR和WKY大鼠的脑微血管ACE相似。在该模型中,微血管ACE不太可能参与高血压的发病机制或并发症。