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Article: Nebivolol induces endothelium-dependent relaxations of canine coronary arteries

TitleNebivolol induces endothelium-dependent relaxations of canine coronary arteries
Authors
Issue Date1991
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1991, v. 17 n. 6, p. 964-969 How to Cite?
AbstractNebivolol is a new β1-antagonist that acutely reduces arterial blood pressure without depressing cardiac function. The present study was designed to determine the effect of nebivolol on coronary arteries. Rings of canine left anterior descending coronary (LAD) artery with or without endothelium were suspended in organ chambers and the isometric tension was recorded. In some experiments, the transmembrane potential of the smooth muscle cells was recorded by electrophysiological methods. During contractions to prostaglandin F(2α), nebivolol induced concentration-dependent relaxations of the coronary arteries. The enantiomer, l-nebivolol, also induced comparable relaxations; however, d-nebivolol induced smaller relaxations. The relaxations induced by nebivolol and its enantiomer were significantly larger in tissues with than in those without endothelium. The differences between tissues with and without endothelium were abolished by nitro-L-arginine (3 x 10-5 M) or methylene blue (10-5 M). The nebivolol-induced relaxations were not affected by indomethacin (10-5 M), phentolamine (5 x 10-6 M), propranolol (5 x 10-6 M), or methysergide (3 x 10-6 M). Nebivolol at a subthreshold concentration for inducing relaxation (3 x 10-7 M) did not significantly affect endothelium-dependent relaxations to acetylcholine but potentiated ADP-induced endothelium-dependent relaxations. The potentiation is stereoselective for l-nebivolol. Nebivolol induced a small hyperpolarization of the coronary smooth muscle with endothelium (1 mV). These observations demonstrate that (a) nebivolol induces relaxations of canine coronary arteries that are mainly mediated by endothelium-derived relaxing factor(s); these effects are not related to the α- and β-adrenergic- or serotonergic 5-HT1- and 5-HT2-blocking properties of the compound; (b) nebivolol potentiates ADP-induced endothelium-dependent relaxations; and (c) l-nebivolol is more potent than d-nebivolol in inducing and potentiating endothelium-dependent relaxations.
Persistent Identifierhttp://hdl.handle.net/10722/171018
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorGao, Yen_US
dc.contributor.authorNagao, Ten_US
dc.contributor.authorBond, RAen_US
dc.contributor.authorJanssens, WJen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:51Z-
dc.date.available2012-10-30T06:11:51Z-
dc.date.issued1991en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1991, v. 17 n. 6, p. 964-969en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/171018-
dc.description.abstractNebivolol is a new β1-antagonist that acutely reduces arterial blood pressure without depressing cardiac function. The present study was designed to determine the effect of nebivolol on coronary arteries. Rings of canine left anterior descending coronary (LAD) artery with or without endothelium were suspended in organ chambers and the isometric tension was recorded. In some experiments, the transmembrane potential of the smooth muscle cells was recorded by electrophysiological methods. During contractions to prostaglandin F(2α), nebivolol induced concentration-dependent relaxations of the coronary arteries. The enantiomer, l-nebivolol, also induced comparable relaxations; however, d-nebivolol induced smaller relaxations. The relaxations induced by nebivolol and its enantiomer were significantly larger in tissues with than in those without endothelium. The differences between tissues with and without endothelium were abolished by nitro-L-arginine (3 x 10-5 M) or methylene blue (10-5 M). The nebivolol-induced relaxations were not affected by indomethacin (10-5 M), phentolamine (5 x 10-6 M), propranolol (5 x 10-6 M), or methysergide (3 x 10-6 M). Nebivolol at a subthreshold concentration for inducing relaxation (3 x 10-7 M) did not significantly affect endothelium-dependent relaxations to acetylcholine but potentiated ADP-induced endothelium-dependent relaxations. The potentiation is stereoselective for l-nebivolol. Nebivolol induced a small hyperpolarization of the coronary smooth muscle with endothelium (1 mV). These observations demonstrate that (a) nebivolol induces relaxations of canine coronary arteries that are mainly mediated by endothelium-derived relaxing factor(s); these effects are not related to the α- and β-adrenergic- or serotonergic 5-HT1- and 5-HT2-blocking properties of the compound; (b) nebivolol potentiates ADP-induced endothelium-dependent relaxations; and (c) l-nebivolol is more potent than d-nebivolol in inducing and potentiating endothelium-dependent relaxations.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_US
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_US
dc.subject.meshAdrenergic Beta-Antagonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBenzopyrans - Pharmacologyen_US
dc.subject.meshCoronary Vessels - Drug Effects - Physiologyen_US
dc.subject.meshDinoprost - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshEthanolamines - Pharmacologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle Relaxation - Drug Effects - Physiologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Cytology - Drug Effects - Physiologyen_US
dc.titleNebivolol induces endothelium-dependent relaxations of canine coronary arteriesen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/00005344-199106000-00016-
dc.identifier.pmid1714022-
dc.identifier.scopuseid_2-s2.0-0025948189en_US
dc.identifier.volume17en_US
dc.identifier.issue6en_US
dc.identifier.spage964en_US
dc.identifier.epage969en_US
dc.identifier.isiWOS:A1991FQ07100016-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridGao, Y=7404706442en_US
dc.identifier.scopusauthoridNagao, T=7401489430en_US
dc.identifier.scopusauthoridBond, RA=7102696356en_US
dc.identifier.scopusauthoridJanssens, WJ=7006876881en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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