Vasodilator response to local hyperinsulinemia.

  title={Vasodilator response to local hyperinsulinemia.},
  author={S. Ueda and J. Petrie and S. Cleland and H. Elliott and J. Connell},
  volume={34 6},
To the Editor: Cardillo et al recently reported that systemic but not local hyperinsulinemia causes nitric oxide (NO)-dependent vasodilatation.1 They suggest that mechanisms stimulated only by systemic but not local hyperinsulinemia contribute to insulin-mediated vasodilatation. We believe that this conclusion is mistaken. The changes in forearm blood flow during systemic and local hyperinsulinemia in their study were not directly comparable. Thus, although similar concentrations of insulin… Expand


Vasodilator response to systemic but not to local hyperinsulinemia in the human forearm.
It is concluded that systemic, but not local, hyperinsulinemia induces vasodilation in the forearm, and the effect of nitric oxide synthase inhibition by NG-monomethyl-L-arginine on the vasodilator and metabolic responses to hyperinsulainemia is assessed. Expand
The vasodilating effect of insulin is dependent on local glucose uptake: a double blind, placebo-controlled study.
The data suggest that local uptake of D-glucose by insulin-sensitive tissues is an important determinant of insulin-mediated vasodilation, and that no augmentation of the vascular effect was observed with coinfusion of L- glucose, the metabolically inactive stereoisomer. Expand
Differential effects of hyperinsulinemia and carbohydrate metabolism on sympathetic nerve activity and muscle blood flow in humans.
It is suggested that in humans hyperinsulinemia per se, rather than insulin-induced stimulation of carbohydrate metabolism, is the main mechanism that triggers both sympathetic activation and vasodilation in skeletal muscle. Expand
Exposure To Elevated D-Glucose Concentrations Modulates Vascular Endothelial Cell Vasodilatory Response
It is suggested that prolonged exposure to pathological high D-glucose concentrations results in an enhanced endothelium-derived relaxing factor formation caused by amplification of agonist-stimulated Ca2+ mobilization in endothelial cells. Expand
Insulin-stimulated glucose transport inhibits Ca2+ influx and contraction in vascular smooth muscle.
It is concluded that insulin-stimulated glucose transport is an early event that leads to decreased Ca2+ influx and contraction in vascular smooth muscle. Expand