Shi S J, Rakugi H, Higashimori K, Higaki J, Mikami H, Ogihara T
Department of Geriatric Medicine, Osaka University Medical School, Japan.
Blood Press Suppl. 1994;5:27-31.
The objectives of the present study were to test the hypothesis that vascular angiotensin II (AII) generation may be negatively regulated by circulating AII in Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), and to clarify the role of this vascular AII in the sustained hypertension seen in SHR following nephrectomy. The mesenteric arteries from kidney-intact and nephrectomised WKY and SHR were perfused, and the level of AII released into the perfusate were measured. The effects of CV-11974, a newly developed nonpeptide AII receptor antagonist, on AII release were examined to investigate the existence of a local feedback system in the blood vessels. Nephrectomy augmented vascular AII release both in WKY and SHR despite the reduction in circulating AII. CV-11974 significantly increased AII release from the mesenteric arteries of kidney-intact rats. There were no significant differences in these responses between WKY and SHR. These results suggest that WKY and SHR share a potent pathway for producing vascular AII in response to the withdrawal of circulating AII, although this pathway is not responsible for the sustained hypertension seen in SHR after nephrectomy.
在Wistar-Kyoto大鼠（WKY）和自发性高血压大鼠（SHR）中，血管血管紧张素II（AII）的生成可能受到循环AII的负调控，并阐明这种血管AII在SHR肾切除术后持续性高血压中的作用。对完整肾脏和肾切除的WKY及SHR的肠系膜动脉进行灌注，并测量灌注液中释放的AII水平。研究新开发的非肽类AII受体拮抗剂CV-11974对AII释放的影响，以探究血管中局部反馈系统的存在。尽管循环AII减少，但肾切除术增加了WKY和SHR中血管AII的释放。CV-11974显著增加了完整肾脏大鼠肠系膜动脉的AII释放。WKY和SHR之间的这些反应没有显著差异。这些结果表明，WKY和SHR在循环AII减少时共享一条产生血管AII的有效途径，尽管该途径与SHR肾切除术后的持续性高血压无关。
