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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.

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Release of enzymes from a rat liver lysosome fraction: inhibition by catecholamines and cyclic3', 5'-adenosine monophosphate, stimulation by cholinergic agents and cyclic 3', 5'-guanosine monophosphate.

TL;DR: The data in this report suggest that the inflammatory process can be regulated by the autonomic nervous system through the actions of neurohormones and cyclic nucleotides on the release of enzymes from lysosomes.
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Nitric Oxide: A Unique Endogenous Signaling Molecule in Vascular Biology (Nobel Lecture)

TL;DR: In this article, the authors proposed that the endothelium-derived relaxing factor (EDRF) must be Nitric Oxide (NO) and found that the effects on or actions of EDRF were identical to those of NO.
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17β-Estradiol inhibits NADPH oxidase activity through the regulation of p47phox mRNA and protein expression in THP-1 cells

TL;DR: It is implicate that 17beta-estradiol has an anti-atherosclerotic effects through the improvement of nitric oxide (NO) bioavailability caused by the regulation of superoxide (O(2)(-)) production.
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Neutral protease release from human leukocytes regulated by neurohormones and cyclic nucleotides.

TL;DR: Enzymes released from leukocytes during phagocytosis of particulate material are inhibited by cyclic 3′,5′-adenosine monophosphate and prostaglandin E1, which raises cyclic AMP levels in certain tissues9 and catecholamines also raise tissue levels of cyclicAMP.
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Nitric oxide: inhibitory effects on endothelial cell calcium signaling, prostaglandin I2 production and nitric oxide synthase expression.

TL;DR: No, when produced in large amounts, can inhibit agonist-induced Ca2+ responses independently of cyclic GMP, reduce the production of endothelium-derived relaxing factors (EDRFs) and interfere with endothelial NO synthase protein expression.