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Biosynthesis and Metabolism of Endothelium-Derived Nitric Oxide

Biosynthesis and Metabolism of Endothelium-Derived Nitric Oxide Studies on the biological actions of nitric oxide (NO) essentially began with the observations that NO gas, generated from an acidified nitrite solution, activated crude soluble preparations of guanylate cyclase (1, 2). In a series of pioneering experiments, Murad et al observed that NO could account for the ability of numerous chemically diverse, nitrogen-containing compounds to activate cytosolic guanylate cyclase and elevate tissue levels of cyclic GMP (3). The mechanism of heme-dependent activation of guanylate cyclase by NO and labile nitroso compounds that spontaneously liberate NO was dis­ covered by Craven & DeRubertis inhibitor of platelet aggregation came from our laboratory (4). The first observation that NO is a potent (5). In addition, we extended the initial hypothesis on the requirement of tissue thiols for the vasodilator action of nitroglycerin, forwarded by Needleman et al (6, 7), with the findings that nitroglycerin reacts with cysteine to yield S-nitrosocysteine, which is a labile but potent vascular smooth-muscle relaxant that works through the action of liberated NO (8). S-Nitrosothiols were found to be labile precursors of NO that activate cytoplasmic or cytosolic guanylate cyclase, elevate vascular and platelet levels of cyclic GMP, and cause vascular smooth-muscle relaxation, inhibition of platelet http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Pharmacology and Toxicology Annual Reviews

Biosynthesis and Metabolism of Endothelium-Derived Nitric Oxide

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References (44)

Publisher
Annual Reviews
Copyright
Copyright 1990 Annual Reviews. All rights reserved
Subject
Review Articles
ISSN
0362-1642
eISSN
1545-4304
DOI
10.1146/annurev.pa.30.040190.002535
pmid
2188578
Publisher site
See Article on Publisher Site

Abstract

Studies on the biological actions of nitric oxide (NO) essentially began with the observations that NO gas, generated from an acidified nitrite solution, activated crude soluble preparations of guanylate cyclase (1, 2). In a series of pioneering experiments, Murad et al observed that NO could account for the ability of numerous chemically diverse, nitrogen-containing compounds to activate cytosolic guanylate cyclase and elevate tissue levels of cyclic GMP (3). The mechanism of heme-dependent activation of guanylate cyclase by NO and labile nitroso compounds that spontaneously liberate NO was dis­ covered by Craven & DeRubertis inhibitor of platelet aggregation came from our laboratory (4). The first observation that NO is a potent (5). In addition, we extended the initial hypothesis on the requirement of tissue thiols for the vasodilator action of nitroglycerin, forwarded by Needleman et al (6, 7), with the findings that nitroglycerin reacts with cysteine to yield S-nitrosocysteine, which is a labile but potent vascular smooth-muscle relaxant that works through the action of liberated NO (8). S-Nitrosothiols were found to be labile precursors of NO that activate cytoplasmic or cytosolic guanylate cyclase, elevate vascular and platelet levels of cyclic GMP, and cause vascular smooth-muscle relaxation, inhibition of platelet

Journal

Annual Review of Pharmacology and Toxicology – Annual Reviews

Published: Apr 1, 1990

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