作者: Frank M. Faraci
DOI: 10.1161/01.RES.0000250961.47984.80
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摘要: See related article, pages 1132–1140 Nitric oxide (NO) plays a major role in both vascular and neural biology health disease. This concept is exemplified when one examines the of NO brain cerebral circulation. potent vasodilator, blood vessels are normally exposed to from 2 sources—endothelium neurons. Acting as messenger molecule, mediates majority endothelium-dependent responses brain.1 The source this endothelial isoform synthase (eNOS). prominent for has been observed variety multiple species including humans.1–3 Through signaling mechanism, influences resting tone varied stimuli, agonists increases flow (Figure).1,4,5 In addition, eNOS inhibits vasoconstrictor vasospasm6–8 can affect permeability endothelium, blood-brain barrier (Figure).9 growth or hypertrophy (Figure),10 structural change that have functional consequences by impairing maximal vasodilator capacity. Impairment NO-mediated key underlying mechanism dysfunction diverse forms disease aging.1,11–13 these eNOS-dependent mechanisms presence cardiovascular risk factors may contribute …