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Endogenous nitric oxide: physiology, pathology and clinical relevance

Endogenous nitric oxide: physiology, pathology and clinical relevance REVIEW Endogenous nitric oxide: physiology, pathology and clinical relevance S. MONCADA & E. A. HIGGS, The Wellcome Research Laboratories, Beckenham, Kent, UK Received 2 May 1991 Introduction The formation of nitric oxide (NO) from the amino acid L-arginine not only explains the biological properties of the so-called endothelium-derived relaxing factor (EDRF) but also accounts for the stimulation of the soluble guanylate cyclase in a number of tissues such as the platelet and the brain. Furthermore, NO is a cytotoxic factor released by murine macrophages and other cells following immunological activation. Nitric oxide is synthesized by an enzyme, the N O synthase, of which two types have been identified. One type is constitutive and is responsible for the release of NO for physiological transduction purposes, while the other is induced by cytokines and releases NO as part of the immunological response. The constitutive nitric oxide synthase 1. The vusculature EDRF [I] is a labile humoral substance which accounts for the vascular relaxation induced by acetylcholine (ACh) and other endothelium-dependent vasodilators. It also inhibits platelet aggregation [2,3] and adhesion [4], all of which actions are mediated via stimulation of the soluble guanylate cyclase. The chemical nature of EDRF has been http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Clinical Investigation Wiley

Endogenous nitric oxide: physiology, pathology and clinical relevance

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Publisher
Wiley
Copyright
Copyright © 1991 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0014-2972
eISSN
1365-2362
DOI
10.1111/j.1365-2362.1991.tb01383.x
Publisher site
See Article on Publisher Site

Abstract

REVIEW Endogenous nitric oxide: physiology, pathology and clinical relevance S. MONCADA & E. A. HIGGS, The Wellcome Research Laboratories, Beckenham, Kent, UK Received 2 May 1991 Introduction The formation of nitric oxide (NO) from the amino acid L-arginine not only explains the biological properties of the so-called endothelium-derived relaxing factor (EDRF) but also accounts for the stimulation of the soluble guanylate cyclase in a number of tissues such as the platelet and the brain. Furthermore, NO is a cytotoxic factor released by murine macrophages and other cells following immunological activation. Nitric oxide is synthesized by an enzyme, the N O synthase, of which two types have been identified. One type is constitutive and is responsible for the release of NO for physiological transduction purposes, while the other is induced by cytokines and releases NO as part of the immunological response. The constitutive nitric oxide synthase 1. The vusculature EDRF [I] is a labile humoral substance which accounts for the vascular relaxation induced by acetylcholine (ACh) and other endothelium-dependent vasodilators. It also inhibits platelet aggregation [2,3] and adhesion [4], all of which actions are mediated via stimulation of the soluble guanylate cyclase. The chemical nature of EDRF has been

Journal

European Journal of Clinical InvestigationWiley

Published: Aug 1, 1991

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