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Endothelial Dysfunction in Cardiovascular Diseases: The Role of Oxidant Stress

Circulation Research · 2000 · Vol. 87(10) · pp. 840–844
Hua CaiDavid G. Harrison

Abstract

Accumulating evidence suggests that oxidant stress alters many functions of the endothelium, including modulation of vasomotor tone. Inactivation of nitric oxide (NO(.)) by superoxide and other reactive oxygen species (ROS) seems to occur in conditions such as hypertension, hypercholesterolemia, diabetes, and cigarette smoking. Loss of NO(.) associated with these traditional risk factors may in part explain why they predispose to atherosclerosis. Among many enzymatic systems that are capable of producing ROS, xanthine oxidase, NADH/NADPH oxidase, and uncoupled endothelial nitric oxide synthase have been extensively studied in vascular cells. As the role of these various enzyme sources of ROS become clear, it will perhaps be possible to use more specific therapies to prevent their production and ultimately correct endothelial dysfunction.

Nitric Oxide and Endothelin EffectsEicosanoids and Hypertension PharmacologyRenin-Angiotensin System StudiesXanthine oxidaseEndothelial dysfunctionReactive oxygen speciesNADPH oxidaseOxidative stressNitric oxideSuperoxideEndotheliumNitric oxide synthaseMedicine

MeSH terms

AnimalsCardiovascular DiseasesEndothelium, VascularHumansNADH, NADPH OxidoreductasesNitric OxideXanthine OxidaseReactive Oxygen SpeciesOxidative StressNitric Oxide SynthaseNitric Oxide Synthase Type III

Funding

  • National Institutes of Health
Citations
3,781
FWCI
56.33
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References
48
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References
Superoxide anions and hyperoxia inactivate endothelium-derived relaxing factor
American Journal of Physiology-Heart and Circulatory Physiology · 1986 · 1,185 citations
NAD(P)H Oxidase
Circulation Research · 2000 · 2,875 citations
Hypercholesterolemia increases endothelial superoxide anion production.
Journal of Clinical Investigation · 1993 · 1,774 citations
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