Abstract
Recently the relationship between sulfhydryls and cGMP has been discussed in the several biological processes. While captopril, but not enalapril, is a sulfhydryl-containing angiotensin converting enzyme (ACE) inhibitor, we have previously reported that it decreased PGI2 generation in cultured human vascular endothelial cells. So we aimed to investigate the implication of cGMP and sulfhydryls in the regulatory mechanisms of PGI2 generation including with which induced by captopril with reference to Ca++ kinetics, Bradykinin and Ca ionophre A23187 enhanced PGI2 generation, and the cytosolic free Ca++ concentration ([Ca++]i). And 8-bromo cGMP increased intracellular cGMP concentration ([cGMP]i), and decreased PGI2 generation without change in [Ca++]i. Sulfhydryl radical containing compounds such as captopril, N-acetylcysteine and glutathione decreased PGI2 generation via the increased [cGMP]i. However an ACE inhibitor without sulfhydryl radicals, enalapril had no effect on them. Through these results it was suggested that enalapril might be more beneficial than captopril for the management of hypertensive patients with thromboembolic complications, and is was considered to be an important factor whether the vasoactive substances contain the sulfhydryls or not for the examinination of their effects on PGI2 generation.
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