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

Abstract

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

Twenty-five years since the discovery of endothelium-derived relaxing factor (EDRF): does a dysfunctional endothelium contribute to the development of type 2 diabetes?

“…A short 6-min exposure to elevated glucose in healthy young males has been found to activate platelet eNOS via a PKCbeta mediated process that could be mimicked by mannitol, thus suggesting an osmotic mechanism leading to elevations of platelet cGMP and cAMP. These data could at least partially explain the rapid vasodilatation effects of elevated glucose that are reported in vivo (van Veen et al 1999), but, at the same time, reflect the complexities in determining the effects of hyperglycaemia on vascular function (Fleming 2005). …”

“…For example, high local levels of glucose have a vasodilator effect on resistance vessels in skeletal muscle of the forearm that is not modified by local hyperinsulinaemia (van Veen et al 1999). Enhanced blood flow that results from an increase in plasma glucose may be in part due to a glucose-mediated activation of endothelial eNOS (Taubert et al 2004) and in part by, possibly via an osmotic action, activation of platelet eNOS (Massucco et al 2005).…”

Acute effects of glucose and insulin on vascular endothelium

“…While the vasodilating effects of insulin are established [9,10], the direct vascular actions of short-term hyperglycaemia are largely unknown. Studies investigating the effects of high glucose on macrovascular and microvascular perfusion have yielded conflicting results: some have shown attenuated vasodilation [11,12,13,14,15,16], some have demonstrated enhanced vasodilation [17,18,19,20], whereas others found no changes in vascular tone [21,22,23]. The present study was designed to gain deeper insights into the immediate effects of high glucose on endothelial NO formation and vascular tone, and its stimulatory role on the vascular effects of insulin.…”

Cardiovascular and Renal Complications in Obesity and Obesity-Related Medical Conditions: Role of Sympathetic Nervous Activity and Insulin Resistance

“…Insulin causes forearm vasoconstriction in obese, insulin resistant hypertensive humans [Gudbjornsdotti, et al 1998]. On the other hand, van Veen et al [van Veen, et al 1999] found that hyperglycemia induced vasodilation in the forearm, but this vasodilation was not modified by hyperinsulinemia.…”