Open AccessEffects of Angiotensin I Converting Enzyme (ACE)-Related Substances on Prostacyclin Generation and ACE Activity of Human Vascular Endothelial Cells and Rat Aortic Rings
Author(s) -
Masao Nakagawa,
S. Sawada,
Uno M,
Hajime Takamatsu,
Yuji Nakamura,
Yusuke Nakanishi,
Hajime Tsuji,
Takeo Toyoda,
Shin Sasaki,
Kazuki Takeda
Publication year - 1987
Publication title -
journal of cardiovascular pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/00005344-198706107-00022
Subject(s) - captopril , prostacyclin , bradykinin , angiotensin converting enzyme , stimulation , angiotensin ii , medicine , chemistry , contraction (grammar) , renin–angiotensin system , endocrinology , enzyme , ace inhibitor , biochemistry , receptor , blood pressure
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(-3) M) 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.