L
Louis J. Ignarro
Researcher at University of California, Los Angeles
Publications - 335
Citations - 47353
Louis J. Ignarro is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Nitric oxide & Nitric oxide synthase. The author has an hindex of 106, co-authored 335 publications receiving 46008 citations. Previous affiliations of Louis J. Ignarro include Boston University & Konkuk University.
Papers
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Journal ArticleDOI
Signal transduction mechanisms involving nitric oxide
TL;DR: L'interaction entre l'oxyde nitrique (NO) and le groupement prosthetique de l'heme de la guanylate cyclase cytosolique est responsable du mecanisme de signal transduction qui provoque la biosynthese de GMP cyclique dans les cellules cibles suite a uen stimulus exterieur.
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Shear stress-induced release of nitric oxide from endothelial cells grown on beads.
TL;DR: Observations indicate that fluid shear stress causes the generation of EDRF with properties of nitric oxide from aortic endothelial cells and that the bioassay system described may be useful for studying the mechanism of mechanochemical coupling that leads to Nitric oxide generation.
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Free radical biology and medicine: it's a gas, man!
William A. Pryor,Kendall N. Houk,Christopher S. Foote,Jon M. Fukuto,Louis J. Ignarro,Giuseppe L. Squadrito,Kelvin J.A. Davies +6 more
TL;DR: Gasses that can affect oxidative stress and that themselves may be radicals are reviewed, fearing that many of the gasses discussed in this review will induce transient adaptive responses in gene expression that enable cells and tissues to survive.
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Basal release of nitric oxide from aortic rings is greater in female rabbits than in male rabbits: implications for atherosclerosis
TL;DR: It is established that basal NO release from endothelium-intact aortic rings depends on circulating estradiol concentration and offers an explanation for the protective effect of estradio against the development of atherosclerosis.
Journal Article
Relaxation of bovine coronary artery and activation of coronary arterial guanylate cyclase by nitric oxide, nitroprusside and a carcinogenic nitrosoamine.
TL;DR: The findings that inhibitors of NO-induced relaxation of coronary artery also inhibit coronary arterial guanylate cyclase activation suggest that cyclic GMP formation may be associated with coronary arteria smooth muscle relaxation.