Cerebrovascular nitrosative stress mediates neurovascular and endothelial dysfunction induced by angiotensin II.

Cerebrovascular nitrosative stress mediates neurovascular and endothelial dysfunction induced by angiotensin II. Research Abstract Details 

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Cerebrovascular nitrosative stress mediates neurovascular and endothelial dysfunction induced by angiotensin II. Abstract Text:

Helene Girouard,Laibaik Park,Josef Anrather,Ping Zhou,Costantino Iadecola,

OBJECTIVE: Angiotensin II (AngII) disrupts the regulation of the cerebral circulation through superoxide, a reactive oxygen species (ROS) generated by a nox2-containing NADPH oxidase. We tested the hypothesis that AngII-derived superoxide reacts with nitric oxide (NO) to form peroxynitrite, which, in turn, contributes to the vascular dysfunction. METHODS AND RESULTS: Cerebral blood flow (CBF) was monitored by laser Doppler flowmetry in the neocortex of anesthetized mice equipped with a cranial window. AngII (0.25+/-0.02 microg/kg/min; intravenous for 30 to 45 minutes) attenuated the cerebral blood flow (CBF) increase produced by topical application of the endothelium-dependent vasodilator acetylcholine (-43+/-1%) and by whisker stimulation (-47+/-1%). AngII also increased the nitration marker 3-nitrotyrosine (3-NT) in cerebral blood vessels, an effect dependent on NO and nox2-derived ROS. Both the cerebrovascular effects of AngII and the nitration were attenuated by pharmacological inhibition or genetic inactivation of NO synthase. The nitration inhibitor uric acid or the peroxynitrite decomposition catalyst FeTPPS abolished AngII-induced cerebrovascular nitration and prevented the cerebrovascular effects of AngII. CONCLUSIONS: These findings provide evidence that peroxynitrite, formed from NO and nox2-derived superoxide, contributes to the deleterious cerebrovascular effects of AngII. Inhibitors of peroxynitrite action may be valuable tools to counteract the deleterious cerebrovascular effects of AngII-induced hypertension.

Cerebrovascular nitrosative stress mediates neurovascular and endothelial dysfunction induced by angiotensin II. Publishing Authors By Initials

H Girouard,L Park,J Anrather,P Zhou,C Iadecola,

For similar animal structures: vibrissae research abstracts see: animal structures: vibrissae research

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Cerebrovascular nitrosative stress mediates neurovascular and endothelial dysfunction induced by angiotensin II. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Arteriosclerosis, thrombosis, and vascular biology

VOLUME: 27

Page Numbers: 303-9

Journal Abbreviation: Arterioscler. Thromb. Vasc. Bi

ISSN: 1524-4636

DAY: 30

MONTH: 11

YEAR: 2006

Cerebrovascular nitrosative stress mediates neurovascular and endothelial dysfunction induced by angiotensin II. Information

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LANGUAGE: eng

NlmUniqueID: 9505803

Cerebrovascular nitrosative stress mediates neurovascular and endothelial dysfunction induced by angiotensin II. Keywords Mesh Terms:

KEYWORDS: Vibrissae

MESH TERMS: physiology

Chemical & Substance for Abstract: Cerebrovascular nitrosative stress mediates neurovascular and endothelial dysfunction induced by angiotensin II. Information

Substance Name: Nitric Oxide Synthase

Registry Number: EC 1.14.13.39

Grant and Affiliation Information for Cerebrovascular nitrosative stress mediates neurovascular and endothelial dysfunction induced by angiotensin II.

AFFILIATION: Division of Neurobiology, Weill Medical College of Cornell University, New York, NY 10021, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL18974

ACRONYM: HL

MEDLINETA: Arterioscler Thromb Vasc Biol

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