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Article: Beta-2 adrenergic responses to tulobuterol in airway smooth muscle, vascular smooth muscle and adrenergic nerves

TitleBeta-2 adrenergic responses to tulobuterol in airway smooth muscle, vascular smooth muscle and adrenergic nerves
Authors
Issue Date1988
PublisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.org
Citation
Journal Of Pharmacology And Experimental Therapeutics, 1988, v. 244 n. 1, p. 173-180 How to Cite?
AbstractExperiments were designed to determine the mechanism of action of the bronchodilator drug tulobuterol. Tissues were suspended in organ chambers for isometric tension recording. Tulobuterol caused concentration-dependent relaxations of guinea pig tracheae, canine saphenous veins and canine bronchi; the compound relaxed canine coronary arteries only at high concentrations and did not affect spontaneously beating guinea pig atria. A metabolite of tulobuterol, 4-hydroxytulobuterol, was more potent in relaxing guinea pig tracheae than tulobuterol, salbutamol and isoproterenol. Other metabolites (3-hydroxy-, 5-hydroxy- and 4,5-dihydroxytulobuterol) were less efficacious than 4-hydroxytulobuterol. Both tulobuterol and 4-hydroxytulobuterol acted as partial agonists. The effects of tulobuterol in the saphenous vein (but not in the coronary artery) were antagonized by the selective beta-2 adrenergic blocker ICI 118,551 but were not affected by the selective beta-1 adrenergic inhibitor metoprolol. In bronchi, removal of the epithelium reduced the relaxations caused by tulobuterol. The drug did not inhibit responses of canine bronchi to electrical stimulation of the cholinergic nerves more than those to exogenous acetylcholine. Tulobuterol caused a moderate augmentation of the evoked release of [ 3H]norepinephrine in canine saphenous veins previously incubated with the labeled transmitter. Thus, tulobuterol is a selective beta-2 adrenergic agonist with minimal nonselective inhibitory effect on airway and vascular smooth muscle. It also facilitates adrenergic neurotransmission, which may help to explain its bronchodilator effect in the intact organism. Tulobuterol does not activate beta-1 adrenoceptors and has no direct positive chronotropic effect. A metabolite of tulobuterol, 4-hydroxytulobuterol, is more active than the parent compound.
Persistent Identifierhttp://hdl.handle.net/10722/170902
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRuff, Fen_US
dc.contributor.authorZander, JFen_US
dc.contributor.authorEdoute, Yen_US
dc.contributor.authorSantais, MCen_US
dc.contributor.authorFlavahan, NAen_US
dc.contributor.authorVerbeuren, TJen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:22Z-
dc.date.available2012-10-30T06:11:22Z-
dc.date.issued1988en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1988, v. 244 n. 1, p. 173-180en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/170902-
dc.description.abstractExperiments were designed to determine the mechanism of action of the bronchodilator drug tulobuterol. Tissues were suspended in organ chambers for isometric tension recording. Tulobuterol caused concentration-dependent relaxations of guinea pig tracheae, canine saphenous veins and canine bronchi; the compound relaxed canine coronary arteries only at high concentrations and did not affect spontaneously beating guinea pig atria. A metabolite of tulobuterol, 4-hydroxytulobuterol, was more potent in relaxing guinea pig tracheae than tulobuterol, salbutamol and isoproterenol. Other metabolites (3-hydroxy-, 5-hydroxy- and 4,5-dihydroxytulobuterol) were less efficacious than 4-hydroxytulobuterol. Both tulobuterol and 4-hydroxytulobuterol acted as partial agonists. The effects of tulobuterol in the saphenous vein (but not in the coronary artery) were antagonized by the selective beta-2 adrenergic blocker ICI 118,551 but were not affected by the selective beta-1 adrenergic inhibitor metoprolol. In bronchi, removal of the epithelium reduced the relaxations caused by tulobuterol. The drug did not inhibit responses of canine bronchi to electrical stimulation of the cholinergic nerves more than those to exogenous acetylcholine. Tulobuterol caused a moderate augmentation of the evoked release of [ 3H]norepinephrine in canine saphenous veins previously incubated with the labeled transmitter. Thus, tulobuterol is a selective beta-2 adrenergic agonist with minimal nonselective inhibitory effect on airway and vascular smooth muscle. It also facilitates adrenergic neurotransmission, which may help to explain its bronchodilator effect in the intact organism. Tulobuterol does not activate beta-1 adrenoceptors and has no direct positive chronotropic effect. A metabolite of tulobuterol, 4-hydroxytulobuterol, is more active than the parent compound.en_US
dc.languageengen_US
dc.publisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.orgen_US
dc.relation.ispartofJournal of Pharmacology and Experimental Therapeuticsen_US
dc.subject.meshAdrenergic Fibers - Drug Effectsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBronchi - Drug Effectsen_US
dc.subject.meshCoronary Vessels - Drug Effectsen_US
dc.subject.meshDogsen_US
dc.subject.meshGuinea Pigsen_US
dc.subject.meshHeart Atria - Drug Effectsen_US
dc.subject.meshMetoprolol - Pharmacologyen_US
dc.subject.meshMuscle, Smooth - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshPropanolamines - Pharmacologyen_US
dc.subject.meshReceptors, Adrenergic, Beta - Drug Effectsen_US
dc.subject.meshSaphenous Vein - Drug Effectsen_US
dc.subject.meshTerbutaline - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshTrachea - Drug Effectsen_US
dc.titleBeta-2 adrenergic responses to tulobuterol in airway smooth muscle, vascular smooth muscle and adrenergic nervesen_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.pmid2826765-
dc.identifier.scopuseid_2-s2.0-0023931468en_US
dc.identifier.volume244en_US
dc.identifier.issue1en_US
dc.identifier.spage173en_US
dc.identifier.epage180en_US
dc.identifier.isiWOS:A1988L779600026-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridRuff, F=7005143443en_US
dc.identifier.scopusauthoridZander, JF=7102225390en_US
dc.identifier.scopusauthoridEdoute, Y=35564584000en_US
dc.identifier.scopusauthoridSantais, MC=6701911004en_US
dc.identifier.scopusauthoridFlavahan, NA=7006398882en_US
dc.identifier.scopusauthoridVerbeuren, TJ=7007006534en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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