Linked Life Data

9007848

Source:http://linkedlifedata.com/resource/pubmed/id/9007848

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-6-9
pubmed:abstractText
In isolated hearts the inotropic response to the beta-adrenoceptor agonist isoproterenol is known to be abolished after ischaemia and reperfusion. The aim of this study was to investigate whether at decreased glucose levels the beta-adrenoceptor-mediated responses in vascular smooth muscle would be depressed, since low glucose conditions mimic the influence of ischaemia. Accordingly, we investigated the influence of low glucose levels in the extracellular space on the vasorelaxation induced by isoproterenol and salbutamol in rat isolated thoracic aortic ring preparations with an intact endothelium and we attempted to further analyze the underlying mechanisms. Therefore, forskolin, dibutyryl-cAMP and glibenclamide (an ATP-sensitive K(+)-channel blocker) were studied as well. In a glucose-free medium the concentration-response curve for isoproterenol was shifted to the left compared to that obtained under normal glucose conditions. The maximal relaxation induced by isoproterenol was not affected by the absence of glucose. In contrast, the maximal relaxation induced by salbutamol in glucose-free medium decreased by 50% compared to that obtained under normal glucose conditions. Glibenclamide caused a concentration-dependent decrease of the maximum relaxation by isoproterenol in a glucose-free medium, but had no effect under normal glucose conditions. Glibenclamide did not influence the concentration-response curves for salbutamol, neither in the presence nor in the absence of glucose in the medium. The relaxation caused by forskolin and dibutyryl-cAMP was not influenced by glibenclamide in a medium devoid of glucose. In endothelium-denuded preparations glibenclamide did not affect isoproterenol-induced responses neither in the presence nor in the absence of glucose. It is concluded that beta-adrenoceptor stimulation opens ATP-sensitive potassium channels under conditions of impaired ATP-metabolism by a cAMP-independent pathway, which needs an intact endothelium.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0028-1298
pubmed:author
pubmed:issnType
Print
pubmed:volume
355
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
97-102
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Contribution of ATP-sensitive potassium channels to beta-adrenoceptor-mediated responses.
pubmed:affiliation
Department of Pharmacotherapy, University of Amsterdam, The Netherlands.
pubmed:publicationType
Journal Article, In Vitro