Elevated glucose promotes generation of endothelium-derived vasoconstrictor prostanoids in rabbit aorta.

“…in pial arterioles of diabetic rats in vivo (Mayhan et al, 1991) and in diabetic isolated aorta (Shimizu et al, 1993;Tesfamariam et al, 1989). Similar mechanisms may play a role after in vitro exposure of rabbit aorta to high glucose concentrations (Tesfamariam et al, 1990). These EDCFs are thought to be released together with the EDRFs and oppose their e ects on the smooth muscle cells.…”

Section: Mechanisms Of Impaired Endothelium-dependent Vasodilatation mentioning

confidence: 95%

Endothelial dysfunction in diabetes

Vriese

Verbeuren

Voorde

et al. 2000

British J Pharmacology

997

769

View full text Add to dashboard Cite

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.

show abstract

“…In experimental studies blood vessels have usually been investigated after at least 60-min incubation at high glucose concentrations, and mainly impaired vasodilator responses were observed. [8][9][10][11] The type of vascular bed studied is also an important determinant. In human retinal blood vessels hyperglycaemia acutely reduces blood flow, 5 while in diabetic children chronically elevated blood glucose levels are associated with retinal vasodilation that precedes the development of overt diabetic retinopathy.…”

Section: Does Glucose Induce Vasodilation or Vasoconstriction?mentioning

confidence: 99%

“…Acutely, it seems that glucose may stimulate the production of nitric oxide, 24,25 however, it may also act indirectly via increased production of insulin. Longer lasting high glucose levels may reduce vascular tone via several mechanisms like, reduced production of nitric oxide, 7 generation of reactive oxygen species, 8 production of vasoconstrictive prostanoids, 9 formation of advanced glycosylation end-products, 10 or release of endothelin. 11 In experimental studies these mechanisms may be easier to demonstrate than in vivo and especially in men where many homeostasis-regulating systems may counteract the effects of longer lasting periods of hyperglyceaemia.…”

Section: Does Glucose Induce Vasodilation or Vasoconstriction?mentioning

confidence: 99%

“…6 The acute effect of hyperglycaemia in combination with acute hyperinsulinaemia on vascular tone in humans is largely unknown. Most experimental studies suggest that hyperglycaemia has vasoconstrictive effects via several mechanisms like: a reduction in the production of nitric oxide, 7 generation of reactive oxygen species, 8 production of vasoconstrictive prostanoids, 9 formation of advanced glycosylation endproducts, 10 and release of endothelin. 11 Therefore, we reasoned that hyperglycaemia itself may induce vasoconstriction and reduce the vasodilating effect of insulin.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Acute hyperglycaemia in the forearm induces vasodilation that is not modified by hyperinsulinaemia

Veen¹,

Frölich

1999

J Hum Hypertens

View full text Add to dashboard Cite

Objective: To evaluate whether acute elevations of local plasma glucose concentrations could influence forearm blood flow (FBF) and how this interacts with local hyperinsulinaemia in healthy volunteers. Methods: Using the perfused forearm technique, in random order, glucose 20% or saline 0.9% as a control was infused in three dose steps (0.3, 1.0, and 3.0 ml/min) for 5 min each in eight healthy men. The infusion experiments were repeated, in random order, during local hyperinsulinaemia by intra-arterial infusion of insulin 0.05 mU/kg/min. The ratio of FBF of the infused over the FBF in the control arm (FR) was measured at 15-sec intervals during the infusions. Results: Glucose infusion increased the FR dosedependently by 172% ± 39% (M ± SE) at the highest dose (P Ͻ 0.01). During hyperinsulinaemia the glucoseinduced increase in FR was significantly (P Ͻ 0.01) less, 96% ± 26%, however, when changes in FR or forearm

show abstract

Elevated glucose promotes generation of endothelium-derived vasoconstrictor prostanoids in rabbit aorta.

Cited by 341 publications

References 14 publications

Superoxide as a Messenger of Endothelial Function

Superoxide as a Messenger of Endothelial Function

Endothelial dysfunction in diabetes

Acute hyperglycaemia in the forearm induces vasodilation that is not modified by hyperinsulinaemia

Contact Info

Product

Resources

About