Endothelium‐derived relaxing and contracting factors

Furchgott, Robert F.; Vanhoutte, Paul M.

doi:10.1096/fasebj.3.9.2545495

Cited by 1,833 publications

(928 citation statements)

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“…Previous reports ascribing an inhibitory role to cyclic GMP using methylene blue do not contradict our conclusion, because this dye, besides blocking guanylyl cyclase, inhibits nitric oxide synthase at even higher potency than guanylyl cyclase [14]. Moreover, the dye stimulates the production of superoxide anion [25]. Both these actions will reduce the tissue NO concentration, so that the observed effect of methylene blue could also be due to changes in NO rather than cyclic GMP levels.…”

Section: Discussioncontrasting

confidence: 46%

Novel guanylyl cyclase inhibitor, ODQ reveals role of nitric oxide, but not of cyclic GMP in endothelin‐1 secretion

1995

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Section: Discussioncontrasting

confidence: 46%

Novel guanylyl cyclase inhibitor, ODQ reveals role of nitric oxide, but not of cyclic GMP in endothelin‐1 secretion

1995

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“…Normal endothelial cells maintain a delicate balance in the vascular between vasoconstriction and vasodilation [Kuo et al, 1988;Unthank et al, 1996;Furchgott and Vanhoutte, 1998]. Endothelium-derived NO (EDNO) is now recognized as a potent vasodilating substance, which modulates endothelium-dependent vasodilator responses.…”

Section: Vascular Endothelium and Nitric Oxide Synthesismentioning

confidence: 99%

Mechanisms of endothelial dysfunction with development of type 1 diabetes mellitus: Role of insulin and C‐peptide

Joshua

Zhang

Falcone

et al. 2005

J of Cellular Biochemistry

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Complications associated with insulin-dependent diabetes mellitus (type-1diabetes) primarily represent vascular dysfunction that has its origin in the endothelium. While many of the vascular changes are more accountable in the late stages of type-1diabetes, changes that occur in the early or initial functional stages of this disease may precipitate these later complications. The early stages of type-1diabetes are characterized by a diminished production of both insulin and C-peptide with a significant hyperglycemia. During the last decade numerous speculations and theories have been developed to try to explain the mechanisms responsible for the selective changes in vascular reactivity and/or tone and the vascular permeability changes that characterize the development of type-1diabetes. Much of this research has suggested that hyperglycemia and/or the lack of insulin may mediate the observed functional changes in both endothelial cells and vascular smooth muscle. Recent studies suggest several possible mechanisms that might be involved in the observed decreases in vascular nitric oxide (NO) availability with the development of type-1 diabetes. In addition more recent studies have indicated a direct role for both endogenous insulin and C-peptide in the amelioration of the observed endothelial dysfunction. These results suggest a synergistic action between insulin and C-peptide that facilitates increase NO availability and may suggest new clinical treatment modalities for type-1 diabetes mellitus.

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“…Endothelial cells actively regulate basal vascular tone and vascular reactivity in physiological and pathological conditions, by responding to mechanical forces and neurohumoral mediators with the release of a variety of relaxing and contracting factors (Furchgott & Vanhoutte, 1989). The endothelium-derived relaxing factors (EDRFs) include nitric oxide (NO), prostacyclin and an, as yet elusive, endotheliumderived hyperpolarizing factor (EDHF) (Feletou & Vanhoutte, 1999).…”

Section: Introductionmentioning

confidence: 99%

Endothelial dysfunction in diabetes

Vriese

Verbeuren

Voorde

et al. 2000

British J Pharmacology

1,007

769

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Endothelial dysfunction plays a key role in the pathogenesis of diabetic vascular disease. The endothelium controls the tone of the underlying vascular smooth muscle through the production of vasodilator mediators. The endothelium-derived relaxing factors (EDRF) comprise nitric oxide (NO), prostacyclin, and a still elusive endothelium-derived hyperpolarizing factor (EDHF). Impaired endothelium-dependent vasodilation has been demonstrated in various vascular beds of di erent animal models of diabetes and in humans with type 1 and 2 diabetes. Several mechanisms of endothelial dysfunction have been reported, including impaired signal transduction or substrate availibility, impaired release of EDRF, increased destruction of EDRF, enhanced release of endothelium-derived constricting factors and decreased sensitivity of the vascular smooth muscle to EDRF. 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. Correction of these pathways, as well as administration of ACE inhibitors and folate, has been shown to improve endothelium-dependent vasodilation in diabetes. Since the mechanisms of endothelial dysfunction appear to di er according to the diabetic model and the vascular bed under study, it is important to select clinically relevant models for future research of endothelial dysfunction.

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Endothelium‐derived relaxing and contracting factors

Cited by 1,833 publications

References 0 publications

Novel guanylyl cyclase inhibitor, ODQ reveals role of nitric oxide, but not of cyclic GMP in endothelin‐1 secretion

Novel guanylyl cyclase inhibitor, ODQ reveals role of nitric oxide, but not of cyclic GMP in endothelin‐1 secretion

Mechanisms of endothelial dysfunction with development of type 1 diabetes mellitus: Role of insulin and C‐peptide

Endothelial dysfunction in diabetes

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