Journal ArticleDOI
Superoxide anion is an endothelium-derived contracting factor
TLDR
Observations are consistent with the hypothesis that superoxide anion, rather than prostaglandins generated by hydroperoxidase activity of cyclooxygenase, is an endothelium-derived contracting factor in canine cerebral arteries.Abstract:
The calcium ionophore A23187 causes endothelium-dependent contractions in canine basilar arteries. Removal of the endothelium, or treatment with indomethacin or superoxide dismutase (SOD), prevented the endothelium-dependent excitatory effect of the calcium ionophore. Catalase and deferoxamine were without effect. Superoxide anion generated by xanthine plus xanthine oxidase in the presence of catalase caused contractions of the vascular smooth muscle, which were abolished by SOD or heat inactivation of xanthine oxidase. The A23187-induced production of prostaglandins F2 alpha and E2 and thromboxane B2 was abolished by the removal of endothelium and by treatment with indomethacin but was not affected by the presence of SOD plus catalase. These observations are consistent with the hypothesis that superoxide anion, rather than prostaglandins generated by hydroperoxidase activity of cyclooxygenase, is an endothelium-derived contracting factor in canine cerebral arteries.read more
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Journal ArticleDOI
Endothelial dysfunction in diabetes
TL;DR: Correcting the principal mediators of hyperglycaemia‐induced endothelial dysfunction may be activation of protein kinase C, increased activity of the polyol pathway, non‐enzymatic glycation and oxidative stress, as well as administration of ACE inhibitors and folate has been shown to improve endothelium‐dependent vasodilation in diabetes.
Journal ArticleDOI
Role of Superoxide in Angiotensin II–Induced but Not Catecholamine-Induced Hypertension
Jørn Bech Laursen,Sanjay Rajagopalan,Zorina S. Galis,Margaret Tarpey,Bruce A. Freeman,David G. Harrison +5 more
TL;DR: Hypertension caused by chronically elevated angiotensin II is mediated in part by .O2-, likely via degradation of endothelium-derived NO, and may contribute to vascular disease in high renin/angiotens in II states.
Journal ArticleDOI
Endothelial dysfunction: a multifaceted disorder (The Wiggers Award Lecture).
Michel Félétou,Paul M. Vanhoutte +1 more
TL;DR: Endothelial cells synthesize and release various factors that regulate angiogenesis, inflammatory responses, hemostasis, as well as vascular tone and permeability, which contribute to endothelial dysfunction.
Journal ArticleDOI
Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels
Frank M. Faraci,D. D. Heistad +1 more
TL;DR: This review focuses on some physiological mechanisms of cerebral vasodilatation and alteration of these mechanisms by disease states.
Journal ArticleDOI
Vitamin C Improves Endothelium-Dependent Vasodilation by Restoring Nitric Oxide Activity in Essential Hypertension
TL;DR: In essential hypertensive patients, impaired endothelial vasodilation can be improved by the antioxidant vitamin C, an effect that can be reversed by the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine, and these findings support the hypothesis thatNitric oxide inactivation by oxygen free radicals contributes to endothelial dysfunction in essential hypertension.