No role of calcium- and ATP-dependent potassium channels in insulin-induced vasodilation in humans in vivo

Diabetes Metab Res Rev. Mar-Apr 2002;18(2):143-8. doi: 10.1002/dmrr.269.


The mechanism of insulin-induced vasodilation has not been completely clarified, but could be important in future treatment strategies of insulin resistance. Recently, a role for calcium-dependent and ATP-dependent potassium (K(Ca) and K(ATP)) channels in insulin-induced vasodilation has been demonstrated in in vitro studies. A role for these channels has never been confirmed in humans in vivo. Therefore, we investigated the role of these channels in insulin-induced vasodilation in humans in vivo. A hyperinsulinemic euglycemic clamp was combined with intra-arterial infusion of placebo, tetraethylammonium (blocker of K(Ca) channels) or glibenclamide (blocker of K(ATP) channels) in three groups of 12 healthy volunteers. Bilateral forearm blood flow was measured with venous occlusion plethysmography. Systemic hyperinsulinemia induced a 20+/-9% vasodilation (p=0.001). Neither tetraethylammonium nor glibenclamide reduced this vasodilation as compared to placebo. According to the results of the present study, insulin-induced vasodilation seems not to be mediated by the opening of K(Ca) and K(ATP) channels in humans in vivo.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / metabolism*
  • Adult
  • Blood Glucose / metabolism
  • Blood Pressure
  • Body Mass Index
  • Forearm / blood supply
  • Glyburide / pharmacology
  • Humans
  • Insulin / blood
  • Insulin / pharmacology*
  • Potassium Channels / physiology*
  • Potassium Channels, Calcium-Activated / physiology
  • Regional Blood Flow
  • Tetraethylammonium / pharmacology
  • Vasodilation / drug effects
  • Vasodilation / physiology*


  • Blood Glucose
  • Insulin
  • Potassium Channels
  • Potassium Channels, Calcium-Activated
  • Tetraethylammonium
  • Adenosine Triphosphate
  • Glyburide