Open AccessJournal Article
Endothelium-derived relaxing and contracting factors.
Paul M. Vanhoutte,Eber B +1 more
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TLDR
Endothelium‐dependent relaxation of blood vessels is produced by a large number of agents (e.g., acetylcholine, ATP and ADP, substance P, bradykinin, histamine, thrombin, serotonin).Abstract:
Since the description of the essential role of the endothelium in mediating relaxations due to acetylcholine in mammalian arteries, it has become obvious that endothelial cells release several relaxing and contracting substances. The release is activated by a variety of agents including circulating hormones, autacoids, and products liberated by aggregating platelets, but also by changes in shear stress exerted by the blood. There is strong evidence that the major endothelium-derived relaxing factor (EDRF) is the free radical nitric oxide (NO) formed enzymatically from L-arginine. Endothelium-dependent relaxations caused by EDRF are induced through increases in the activity of soluble guanylate cyclase in the smooth muscle. Other relaxing factors, such as prostacyclin and endothelium-derived hyperpolarizing factor (EDHF) contribute to endothelium-dependent relaxations. Beside the recently described and chemically identified peptide endothelin, at least two other endothelium-derived contracting factors appear to exist. The mechanisms by which endothelium-derived contracting factors activate vascular smooth muscle are not yet clear. In certain clinical situations an impairment of the production of EDRF in face of a maintained or augmented release of contracting factors may contribute to the occurrence of localized vasospasm or generalized increases in peripheral resistance.read more
Citations
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Localization of nitric oxide synthase indicating a neural role for nitric oxide
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Cloned and expressed nitric oxide synthase structurally resembles cytochrome P-450 reductase.
David S. Bredt,Paul M. Hwang,Charles E. Glatt,Charles J. Lowenstein,Randall R. Reed,Randall R. Reed,Solomon H. Snyder +6 more
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Peroxynitrite-induced membrane lipid peroxidation : the cytotoxic potential of superoxide and nitric oxide
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Expression of Endothelin-1 in the Lungs of Patients with Pulmonary Hypertension
Adel Giaid,Masashi Yanagisawa,David Langleben,René P. Michel,Robert D. Levy,Hani Shennib,Sadao Kimura,Tomoh Masaki,William P. Duguid,Duncan J. Stewart +9 more
TL;DR: Preliminary results suggest that pulmonary hypertension is associated with the increased expression of endothelin-1 in vascular endothelial cells, suggesting that the local production of endethelin- 1 may contribute to the vascular abnormalities associated with this disorder.
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.
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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.
Masashi Yanagisawa,Hiroki Kurihara,Hiroki Kurihara,Sadao Kimura,Yoko Tomobe,Mieko Kobayashi,Youji Mitsui,Yoshio Yazaki,Katsutoshi Goto,Tomoh Masaki +9 more
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.
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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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Vascular endothelial cells synthesize nitric oxide from L-arginine.
TL;DR: It is demonstrated that NO can be synthesized from L-arginine by porcine aortic endothelial cells in culture and the strict substrate specificity of this reaction suggests that L- arginine is the precursor for NO synthesis in vascular endothelium cells.