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(Circulation Research. 2006;99:1029.)
© 2006 American Heart Association, Inc.

Editorials

Protecting the Brain With eNOS

Run for Your Life

Frank M. Faraci

From the Departments of Internal Medicine and Pharmacology, Cardiovascular Center, University of Iowa Carver College of Medicine, Iowa City.

Correspondence to Frank M. Faraci, PhD, Department of Internal Medicine, E315-GH, University of Iowa, Carver College of Medicine, Iowa City, IA 52242-1081. E-mail frank-faraci@uiowa.edu

See related article, pages 1132–1140

Key Words: endothelium • nitric oxide • cerebral circulation • exercise

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

Nitric oxide (NO) plays a major role in both vascular and neural biology in health and disease. This concept is exemplified when one examines the role of NO in the brain and the cerebral circulation. NO is a potent vasodilator, and blood vessels in the brain are normally exposed to NO from 2 major sources—endothelium and neurons. Acting as a messenger molecule, NO mediates the majority of endothelium-dependent responses in the brain.¹ The source of this NO is the endothelial isoform of NO synthase (eNOS). This prominent role for NO has been observed in a variety of blood vessels from multiple species including humans.^1–3 Through this signaling mechanism, NO influences resting vascular tone and mediates responses to varied stimuli, including endothelium-dependent agonists and increases in blood flow (Figure).^1,4,5 In addition, eNOS inhibits vasoconstrictor responses and cerebral vasospasm^6–8 and can affect permeability of cerebral endothelium, the blood-brain barrier (Figure).⁹ eNOS normally inhibits cerebral vascular growth or hypertrophy (Figure),¹⁰ a structural change that can have functional consequences by impairing of maximal vasodilator capacity. Impairment of NO-mediated signaling is a key underlying mechanism of vascular dysfunction in diverse forms of disease and aging.^1,11–13 Impairment of these eNOS-dependent mechanisms in the presence of cardiovascular risk factors may contribute to reductions in cerebral blood flow, vascular cognitive impairment, and stroke.^12,14

View larger version (19K): [in this window] [in a new window]   Schematic summary of selected effects of endothelium and endothelial NO synthase (eNOS) in cerebral circulation and brain. Activation of eNOS with production of NO decreases vascular tone and increases . . . [Full Text of this Article]

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Circ. Res. 2006 99: 1132-1140. [Abstract] [Full Text] [PDF]

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