ARTICLE: PDF OnlyNakagawa Masao; Sawada, Shohei; Uno, Masashi; Takamatsu, Hajime; Nakamura, Yutaka; Nakanishi, Yasuhiro; Tsuji, Hajime; Toyoda, Takeo; Sasaki, Susumu; Takeda, Kazuo; Ijichi, HamaoJournal of Cardiovascular Pharmacology: 1987 - p 113-115 Free Abstract Summary The effects of angiotensin I (ANG I) converting enzyme (ACE)-related substances on prostacyclin (PGI2) generation were investigated using cultured human vascular endothelial cells (EC) and rat aortic rings. ANG I or bradykinin (BK) increased while captopril decreased PGI2 generation and ACE activity of EC, whereas ANG II was without effect. The enhancement of PGI2 generation induced by ANG I or BK was not affected by the pretreatment with captopril. In rat aortic rings, ANG I, ANG II, and BK enhanced whereas captopril (10-3M) attenuated PGI2 generation. Mechanical stimulation of aortic rings stimulated PGI2 generation. These results suggest that (a) the conversion of ANG I to ANG II did not enhance PGI2 generation in EC: (b) the ANG II stimulated PGI2 generation of aortic rings was partially derived by mechanical stimulation of EC, probably originating from the contraction of smooth muscle cells by ANG II; (c) captopril directly inhibited PGI2 generation; and (d) in EC, the stimulation of PGI2 generation by ANG I or BK is probably regulated by an activating effect on ACE as an autoregulatory mechanism. Copyright © 1987 Wolters Kluwer Health, Inc. All rights reserved.