Cook V I, Wright J W, Wright S A, Harding J W
Department of Veterinary and Comparative Anatomy, Washington State University, Pullman 99164-6520.
Brain Res. 1990 Oct 8;529(1-2):320-3. doi: 10.1016/0006-8993(90)90844-2.
The ability of membrane-associated peptidases from the brains of spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats to metabolize iodinated angiotensin (125I-Ang II) and 125I-Ang III was compared. 125I-Ang II was metabolized to 125I-Ang III and other fragments exclusively by membrane-associated peptidases. In contrast to 125I-Ang III which was effectively degraded by both membrane-associated and residual cytosolic peptidases, 125I-Ang II was unaltered by contaminating cytosolic enzymes. The ability of SHR-derived membranes to metabolize 125I-Ang II and produce 125I-Ang III was enhanced when compared to membranes from WKY rats. No difference was observed in the ability of membrane or cytosolic enzymes from SHR and WKY rats to degrade 125I-Ang III. These data are consistent with an increased availability of Ang III in the brains of SHRs.
比较了自发性高血压大鼠（SHR）和正常血压的Wistar-Kyoto（WKY）大鼠大脑中膜相关肽酶代谢碘化血管紧张素（125I-血管紧张素II）和125I-血管紧张素III的能力。125I-血管紧张素II仅通过膜相关肽酶代谢为125I-血管紧张素III和其他片段。与125I-血管紧张素III不同，125I-血管紧张素III可被膜相关肽酶和残留的胞质肽酶有效降解，而125I-血管紧张素II不受污染的胞质酶影响。与WKY大鼠的膜相比，SHR来源的膜代谢125I-血管紧张素II并产生125I-血管紧张素III的能力增强。SHR和WKY大鼠的膜或胞质酶降解125I-血管紧张素III的能力未观察到差异。这些数据与SHR大脑中血管紧张素III可用性增加一致。
