Linked Life Data

12512696

Source:http://linkedlifedata.com/resource/pubmed/id/12512696

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4 Pt 1
pubmed:dateCreated
2003-1-6
pubmed:abstractText
Nebivolol is a unique beta1-adrenoceptor antagonist which possesses peripheral vasodilator properties dependent on endothelial NO. Nebivolol-induced release of NO was attributed to its L stereoisomer and to its ability to stimulate endothelial beta2, beta3 adrenoceptors or 5-HT1A receptors. Here, in the isolated guinea pig heart we analysed coronary vasodilator potency of L- and D-nebivolol and a possible role of beta2, beta3 adrenoceptors and 5-HT1A receptors in nebivolol-induced vasodilation. Surprisingly, we found that not only L-nebivolol (3-30 x 10(-6) M) but also D-nebivolol (3-30 x 10(-6) M) induced coronary vasodilation, and both responses were inhibited by L-NAME (10(-4) M). In contrast with the stereoisomers of nebivolol, atenolol at the equimolar concentrations did induce slight vasoconstriction. The nonselective beta1/beta2-adrenoceptor antagonist--nadolol (10(-5) M), the selective beta3-adrenoceptor antagonist--L 748337 (10(-6) M) and the 5 HT1A receptor antagonist--NAN 190 (5 x 10(-6) M), none of them inhibited coronary vasodilation induced by D- and L-nebivolol. In summary, in the isolated guinea pig heart both D- and L-nebivolol act as coronary vasodilators. Coronary vasodilation induced by stereoisomers of nebivolol is mediated by endothelium-derived NO and does not depend on beta2, beta3 adrenoceptors or 5 HT1A receptors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0867-5910
pubmed:author
pubmed:issnType
Print
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
615-24
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
No-dependent vasodilation induced by nebivolol in coronary circulation is not mediated by beta-adrenoceptors or by 5 HT1A-receptors.
pubmed:affiliation
Department of Pharmacology, Jagiellonian University School of Medicine, ul. Grzegorzecka 16 31-531 Krakow, Poland. mfschlop@cyf-kr.edu.pl
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't