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

Cardiovascular Research · 1999 · Vol. 43(3) · pp. 562–571
Georg Kojda

Abstract

There is a growing body of evidence suggesting that numerous pathological conditions are associated with increased vascular production of reactive oxygen species. This form of vascular oxidant stress and particularly interactions between NO and oxygen-derived radicals represent a common pathological mechanism present in many so-called risk factors for atherosclerosis. Furthermore, reactive oxygen species seem to serve important cellular signalling mechanisms responsible for many of the features of vascular lesion formation. The mechanisms whereby vascular cells produce reactive oxygen species are only presently coming to light, and almost certainly will prove to be a focus for future therapies.

Nitric Oxide and Endothelin EffectsCardiovascular, Neuropeptides, and Oxidative Stress ResearchEicosanoids and Hypertension PharmacologyReactive oxygen speciesPathologicalOxidative stressDiabetes mellitusVascular diseaseMechanism (biology)OxygenPathophysiologyMedicineHeart failure

MeSH terms

AnimalsCardiovascular DiseasesCoronary DiseaseDiabetes MellitusEndothelium, VascularHeart FailureHumansHypercholesterolemiaHypertensionNitric OxideSuperoxide DismutaseOxidative StressRats
Citations
772
FWCI
20.07
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102
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100%
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References
Expression of phagocyte NADPH oxidase components in human endothelial cells
American Journal of Physiology-Heart and Circulatory Physiology · 1996 · 426 citations
Free radicals mediate endothelial cell dysfunction caused by elevated glucose
American Journal of Physiology-Heart and Circulatory Physiology · 1992 · 560 citations
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Biochemical Society Transactions · 1993 · 674 citations
Inhibition of Mitochondrial Electron Transport by Peroxynitrite
Archives of Biochemistry and Biophysics · 1994 · 692 citations
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