Premium
No role of calcium‐ and ATP‐dependent potassium channels in insulin‐induced vasodilation in humans in vivo
Author(s) -
Abbink Evertine J.,
Walker Annabel J.,
van der Sluijs Henk A.,
Tack Cees J.,
Smits Paul
Publication year - 2002
Publication title -
diabetes/metabolism research and reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.307
H-Index - 110
eISSN - 1520-7560
pISSN - 1520-7552
DOI - 10.1002/dmrr.269
Subject(s) - vasodilation , glibenclamide , medicine , potassium channel , insulin , endocrinology , hyperinsulinemia , in vivo , tetraethylammonium , chemistry , insulin resistance , pharmacology , potassium , diabetes mellitus , biology , microbiology and biotechnology , organic chemistry
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 . Copyright © 2002 John Wiley & Sons, Ltd.