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Interactions between NO and reactive oxygen species: pathophysiological importance in atherosclerosis, hypertension, diabetes and heart failure

Interactions between NO and reactive oxygen species: pathophysiological importance in... Cardiovascular Research 43 (1999) 562–571 www.elsevier.com / locate / cardiores www.elsevier.nl / locate / cardiores Review Interactions between NO and reactive oxygen species: pathophysiological importance in atherosclerosis, hypertension, diabetes and heart failure ab, Georg Kojda , David Harrison ¨¨ , Dusseldorf, Germany Institut f ur Pharmakologie Emory University School of Medicine, 1639 Pierce Drive, 319 WMB, Atlana, GA 30322, USA Received 3 February 1999; accepted 3 May 1999 1. Background: the concept of ‘endothelial dysfunc- deficiency of either the substrate for the enzyme NO tion’ synthase or one of its critical co-factors. Alterations of endothelial cell signaling may impair appropriate activa- tion of the NO synthase in response to neurohumoral or Soon after the discovery of EDRF (endothelium derived mechanical stimuli. In very advanced atherosclerosis, relaxins factor) it became apparent that certain diseases are expression of NO synthase in the endothelium declines, associated with an impairment of endothelium dependent almost certainly reducing endothelium-dependent vascular vasorelaxation. In hypercholesterolemic rabbits and mon- relaxation. Finally, there is substantial evidence that in keys, vasorelaxation to acetylcholine is almost absent (Fig. certain disease conditions, NO production is not altered, 1) or changed into vasoconstriction [1,2]. Similar observa- but its bioavailability is reduced because of http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Cardiovascular Research Oxford University Press

Interactions between NO and reactive oxygen species: pathophysiological importance in atherosclerosis, hypertension, diabetes and heart failure

Kojda, Georg; Harrison, David
Cardiovascular Research , Volume 43 (3) – Aug 15, 1999
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References (145)

Publisher
Oxford University Press
Copyright
Copyright © 1999, European Society of Cardiology
ISSN
0008-6363
eISSN
1755-3245
DOI
10.1016/S0008-6363(99)00169-8
Publisher site
See Article on Publisher Site

Abstract

Cardiovascular Research 43 (1999) 562–571 www.elsevier.com / locate / cardiores www.elsevier.nl / locate / cardiores Review Interactions between NO and reactive oxygen species: pathophysiological importance in atherosclerosis, hypertension, diabetes and heart failure ab, Georg Kojda , David Harrison ¨¨ , Dusseldorf, Germany Institut f ur Pharmakologie Emory University School of Medicine, 1639 Pierce Drive, 319 WMB, Atlana, GA 30322, USA Received 3 February 1999; accepted 3 May 1999 1. Background: the concept of ‘endothelial dysfunc- deficiency of either the substrate for the enzyme NO tion’ synthase or one of its critical co-factors. Alterations of endothelial cell signaling may impair appropriate activa- tion of the NO synthase in response to neurohumoral or Soon after the discovery of EDRF (endothelium derived mechanical stimuli. In very advanced atherosclerosis, relaxins factor) it became apparent that certain diseases are expression of NO synthase in the endothelium declines, associated with an impairment of endothelium dependent almost certainly reducing endothelium-dependent vascular vasorelaxation. In hypercholesterolemic rabbits and mon- relaxation. Finally, there is substantial evidence that in keys, vasorelaxation to acetylcholine is almost absent (Fig. certain disease conditions, NO production is not altered, 1) or changed into vasoconstriction [1,2]. Similar observa- but its bioavailability is reduced because of

Journal

Cardiovascular Research – Oxford University Press

Published: Aug 15, 1999

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