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(Hypertension. 2008;51:31.)
© 2008 American Heart Association, Inc.

Editorial Commentaries

Oxidative Stress, Nitric Oxide Synthase, and Superoxide Dismutase

A Matter of Imbalance Underlies Endothelial Dysfunction in the Human Coronary Circulation

From the Hypertension and Vascular Research Unit, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis-Jewish General Hospital, Montreal, QC, Canada.

Correspondence to Ernesto L. Schiffrin, MD, PhD, FRSC, FRCPC, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis-Jewish General Hospital, 3755 Côte Ste-Catherine Road, #B-127, Montreal, Quebec, Canada H3T 1E2. E-mail ernesto.schiffrin@mcgill.ca

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Endothelial dysfunction is an independent predictor of cardiovascular risk. It is found with aging, and in many conditions associated with increased cardiovascular risk such as hypertension, atherosclerosis, dyslipidemia, diabetes, obesity, smoking, and renal failure, among others.¹ It is characterized by increased permeability, altered endothelium-mediated vasodilatation, increased vascular reactivity, platelet activation and enhanced thrombogenicity, leukocyte adhesion, and monocyte migration. In large measure it results from increased oxidative stress in the vascular wall mostly attributable to activation of vascular reduced nicotinamide adenine dinucleotide (NADPH) oxidase and uncoupling of endothelial nitric oxide synthase (eNOS). There is also increased expression of endothelin-1 (ET-1), an altered balance between the production of vasodilator and vasoconstrictor prostanoids, and induction of adhesion molecules and other proinflammatory mediators.

The degree of endothelial dysfunction has been shown to correlate with cardiovascular outcomes,² and dysfunctional endothelium plays a role in the triggering of cardiovascular events. Although it involves many mediators related to vasoconstriction, vasodilatation, inflammation, and thrombosis, endothelial function was initially described in the Nobel Prize–winning discovery as consisting mainly of vasodilatation induced by cholinergic agents, ultimately leading to the demonstration that NO was one of the main mediators of endothelium-dependent vasodilatation. NO is produced in the blood vessel wall mainly by eNOS, and may be scavenged by excess reactive oxygen species (ROS).³ Thus, the availability of NO to dilate blood vessels depends on the balance between ROS in the vascular wall and the production of NO (Figure). Physiologically, vessels are generally maintained in an NO-mediated quiescent and dilated . . . [Full Text of this Article]

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