Endogenous Inhibitors of Nitric Oxide Synthesis:How  Important Are They?

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Abstract

In animals and humans, inhibition of nitric oxide (NO) production has widespread effects. Reduced activity of the NO:cyclic GMP pathway has been documented in disease states, including hypertension, diabetes and certain types of renal disease. Inhibitors of NO synthesis occur endogenously, and have been implicated in the regulation of the NO pathway in health and disease. Here we review the possible biological roles of endogenous NO synthase inhibitors, with particular reference to renal disease.

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Hypertension in mice lacking the gene for endothelial nitric oxide synthase.

P L Huang, Z. Huang, H Mashimo … (1995)

Nitric oxide (NO), a potent vasodilator produced by endothelial cells, is thought to be the endothelium-dependent relaxing factor (EDRF) which mediates vascular relaxation in response to acetylcholine, bradykinin and substance P in many vascular beds. NO has been implicated in the regulation of blood pressure and regional blood flow, and also affects vascular smooth-muscle proliferation and inhibits platelet aggregation and leukocyte adhesion. Abnormalities in endothelial production of NO occur in atherosclerosis, diabetes and hypertension. Pharmacological blockade of NO production with arginine analogues such as L-nitroarginine (L-NA) or L-N-arginine methyl ester affects multiple isoforms of nitric oxide synthase (NOS), and so cannot distinguish their physiological roles. To study the role of endothelial NOS (eNOS) in vascular function, we disrupted the gene encoding eNOS in mice. Endothelium-derived relaxing factor activity, as assayed by acetylcholine-induced relaxation, is absent, and the eNOS mutant mice are hypertensive. Thus eNOS mediates basal vasodilation. Responses to NOS blockade in the mutant mice suggest that non-endothelial isoforms of NOS may be involved in maintaining blood pressure.

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Journal

Journal ID (publisher-id): EXN

Journal ID (nlm-ta): Nephron Exp Nephrol

Journal ID (doi): 10.1159/issn.1660-2129

Title: Cardiorenal Medicine

Publisher: S. Karger AG

ISSN (Electronic): 1660-2129

Publication date Subscription-year: 1998

Publication date (Print): June 1998

Publication date (Electronic): 22 May 1998

Volume: 6

Issue: 3

Pages: 195-199

Affiliations

Centre for Clinical Pharmacology and Therapeutics, Cruciform Project, and Department of Medicine, University College, London, UK

Article

Publisher ID: 20523 Other ID: Exp Nephrol 1998;6:195–199

DOI: 10.1159/000020523

SO-VID: 3c017a81-ac30-46a1-8e13-7f45af2bcf90

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Endogenous Inhibitors of Nitric Oxide Synthesis:How Important Are They?

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Karger: Nephrology

Most cited references 1

Hypertension in mice lacking the gene for endothelial nitric oxide synthase.

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