The First Robert Furchgott Lecture: From Endothelium-Dependent Relaxation to the  L -Arginine:NO Pathway

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Abstract

Nitric oxide (NO) is released from vascular endothelial cells and fresh vascular tissue in amounts sufficient to account for the biological actions of endothelium-derived relaxing factor. It is synthesized from the terminal guanidino nitrogen atom(s) of L-arginine, a process that is inhibited by N<sup>G</sup>-monomethyl- L-arginine (L-NMMA). Studies using L-NMMA have shown that NO is constantly generated by the vessel wall to maintain vasodilator tone. The L-arginine:NO pathway has now been identified in a number of other cells and tissues, in many of which it acts as the transduction mechanism for stimulation of the soluble guanylate cyclase.

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Journal ID (publisher-id): JVR

Journal ID (nlm-ta): J Vasc Res

Journal ID (doi): 10.1159/issn.1018-1172

Title: Journal of Vascular Research

Publisher: S. Karger AG

ISBN: 978-3-8055-5330-8

ISBN: 978-3-318-01614-7

ISSN (Print): 1018-1172

ISSN (Electronic): 1423-0135

Publication date Subscription-year: 1990

Publication date (Print): 1990

Publication date (Electronic): 23 September 2008

Volume: 27

Issue: 2-5

Pages: 208-217

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Wellcome Research Laboratories, Beckenham, UK

Article

Publisher ID: 158812 Other ID: Blood Vessels 1990;27:208–217

DOI: 10.1159/000158812

SO-VID: 16693389-c174-4c0e-9881-b0daa090c4fe

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The First Robert Furchgott Lecture: From Endothelium-Dependent Relaxation to the L-Arginine:NO Pathway

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Karger: Cardiovascular System

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