NDLI: Role of Nox isoforms in angiotensin II-induced oxidative stress and endothelial dysfunction in brain.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Chrissobolis, Sophocles Banfi, Botond Sobey, Christopher G. Faraci, Frank M.
Description	Country affiliation: United States Author Affiliation: Chrissobolis S ( Department of Internal Medicine, The University of Iowa Carver College of Medicine, Iowa City, IA 52242, USA.)
Abstract	Angiotensin II (Ang II) promotes vascular disease through several mechanisms including by producing oxidative stress and endothelial dysfunction. Although multiple potential sources of reactive oxygen species exist, the relative importance of each is unclear, particularly in individual vascular beds. In these experiments, we examined the role of NADPH oxidase (Nox1 and Nox2) in Ang II-induced endothelial dysfunction in the cerebral circulation. Treatment with Ang II (1.4 mg·kg(-1)·day(-1) for 7 days), but not vehicle, increased blood pressure in all groups. In wild-type (WT; C57Bl/6) mice, Ang II reduced dilation of the basilar artery to the endothelium-dependent agonist acetylcholine compared with vehicle but had no effect on responses in Nox2-deficient (Nox2(-/y)) mice. Ang II impaired responses to acetylcholine in Nox1 WT (Nox1(+/y)) and caused a small reduction in responses to acetylcholine in Nox1-deficient (Nox1(-/y)) mice. Ang II did not impair responses to the endothelium-independent agonists nitroprusside or papaverine in either group. In WT mice, Ang II increased basal and phorbol-dibutyrate-stimulated superoxide production in the cerebrovasculature, and these increases were abolished in Nox2(-/y) mice. Overall, these data suggest that Nox2 plays a relatively prominent role in mediating Ang II-induced oxidative stress and cerebral endothelial dysfunction, with a minor role for Nox1.
File Format	HTM / HTML
ISSN	87507587
e-ISSN	15221601
DOI	10.1152/japplphysiol.00455.2012
Journal	Journal of Applied Physiology
Issue Number	2
Volume Number	113
Language	English
Publisher	American Physiological Society
Publisher Date	2012-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Cerebral Arteries Physiology Cerebrovascular Circulation Endothelium, Vascular Physiopathology Membrane Glycoproteins Metabolism Nadh, Nadph Oxidoreductases Nadph Oxidase Nitric Oxide Synthase Type Iii Oxidative Stress Angiotensin Ii Animals Blood Flow Velocity Blood Pressure Drug Effects Brain Hypertension Chemically Induced Mice Mice, Inbred C57bl Mice, Knockout Protein Isoforms Reactive Oxygen Species Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Sports Science

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