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Mechanisms of Diesel-Induced Endothelial Nitric Oxide Synthase Dysfunction in Coronary Arterioles
Author(s) -
Tom W. Cherng,
Michael L. Paffett,
Olan JacksonWeaver,
Matthew J. Campen,
Benjimen R. Walker,
Nancy L. Kanagy
Publication year - 2010
Publication title -
environmental health perspectives
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.257
H-Index - 282
eISSN - 1552-9924
pISSN - 0091-6765
DOI - 10.1289/ehp.1002286
Subject(s) - nitric oxide synthase , medicine , nitric oxide , vasodilation , coronary arteries , endothelial dysfunction , vasoconstriction , endocrinology , acetylcholine , superoxide , chemistry , cardiology , anesthesia , artery , biochemistry , enzyme
Increased air pollutants correlate with increased incidence of cardiovascular disease potentially due to vascular dysfunction. We have reported that acute diesel engine exhaust (DE) exposure enhances vasoconstriction and diminishes acetylcholine (ACh)-induced dilation in coronary arteries in a nitric oxide synthase (NOS)-dependent manner. We hypothesize that acute DE inhalation leads to endothelial dysfunction by uncoupling NOS.

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