Linked Life Data

11994906

Source:http://linkedlifedata.com/resource/pubmed/id/11994906

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2002-5-23
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1520-7552
pubmed:author
pubmed:copyrightInfo
Copyright 2002 John Wiley & Sons, Ltd.
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
143-8
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:articleTitle
No role of calcium- and ATP-dependent potassium channels in insulin-induced vasodilation in humans in vivo.
pubmed:affiliation
Division of General Internal Medicine, Department of Medicine, University Medical Centre, Nijmegen, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't