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Open AccessJournal ArticleDOI

Biological actions and properties of endothelium-derived nitric oxide formed and released from artery and vein.

Louis J. Ignarro
- 01 Jul 1989 - 
- Vol. 65, Iss: 1, pp 1-21
TLDR
Article de synthese traitant de la pharmacologie de l'oxyde nitrique, du facteur EDRF and du GMP cyclique dans les vaisseaux sanguins and les thrombocytes, de la formation, de the liberation and du metabolisme de l’endothelium derived NO (EDNO).
Abstract
Article de synthese traitant de la pharmacologie de l'oxyde nitrique, du facteur EDRF et du GMP cyclique dans les vaisseaux sanguins et les thrombocytes, de l'isolation et de l'identification du facteur EDRF comme de l'oxyde nitrique, et de la formation, de la liberation et du metabolisme de l'endothelium derived NO (EDNO)

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Citations
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Journal ArticleDOI

Biochemistry of nitric oxide and its redox-activated forms

TL;DR: The integration of this chemistry with current perspectives of NO biology illuminates many aspects of NO biochemistry, including the enzymatic mechanism of synthesis, the mode of transport and targeting in biological systems, the means by which its toxicity is mitigated, and the function-regulating interaction with target proteins.
Journal ArticleDOI

Inhaled Nitric Oxide for the Adult Respiratory Distress Syndrome

TL;DR: Inhalation of nitric oxide by patients with severe adult respiratory distress syndrome reduces the pulmonary-artery pressure and increases arterial oxygenation by improving the matching of ventilation with perfusion, without producing systemic vasodilation.
Journal ArticleDOI

S-nitrosylation of proteins with nitric oxide: synthesis and characterization of biologically active compounds

TL;DR: It is demonstrated that S-nitroso proteins form readily under physiologic conditions and possess EDRF-like effects of vasodilation and platelet inhibition, suggesting that S -nitrosothiol groups in proteins may serve as intermediates in the cellular metabolism of NO and raise the possibility of an additional type of cellular regulatory mechanism.
Journal ArticleDOI

Inhaled nitric oxide. A selective pulmonary vasodilator reversing hypoxic pulmonary vasoconstriction.

TL;DR: Breathing 80 ppm NO for 3 hours did not increase either methemoglobin or extravascular lung water levels or modify lung histology compared with those in control lambs.
References
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Journal ArticleDOI

The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine

TL;DR: It is demonstrated that relaxation of isolated preparations of rabbit thoracic aorta and other blood vessels by ACh requires the presence of endothelial cells, and that ACh, acting on muscarinic receptors of these cells, stimulates release of a substance(s) that causes relaxation of the vascular smooth muscle.
Journal ArticleDOI

Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor

TL;DR: NO released from endothelial cells is indistinguishable from EDRF in terms of biological activity, stability, and susceptibility to an inhibitor and to a potentiator.
Journal ArticleDOI

A novel potent vasoconstrictor peptide produced by vascular endothelial cells.

TL;DR: Cloning and sequencing of preproendothelin complementary DNA shows that mature endothelin is generated through an unusual proteolytic processing, and regional homologies to a group of neurotoxins suggest that endothelins is an endogenous modulator of voltage-dependent ion channels.
Journal ArticleDOI

Involvement of the Superoxide Anion Radical in the Autoxidation of Pyrogallol and a Convenient Assay for Superoxide Dismutase

TL;DR: The autoxidation of pyrogallol was investigated in the presence of EDTA in the pH range 7.9–10.6, indicating an almost total dependence on the participation of the superoxide anion radical, O2·−, in the reaction.
Journal ArticleDOI

Endothelium-derived relaxing factor produced and released from artery and vein is nitric oxide.

TL;DR: The vascular effects of EDRF released from perfused bovine intrapulmonary artery and vein were compared with the effects of NO delivered by superfusion over endothelium-denuded arterial and venous strips arranged in a cascade to determine whether nitric oxide (NO) is responsible for the vascular smooth muscle relaxation elicited by endothelia-derived relaxing factor (EDRF).
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