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

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 KATP 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. Copyright (C) 2002 John Wiley Sons, Ltd.