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Article: Mechanisms of impaired β-adrenoceptor-induced airway relaxation by interleukin-1β in vivo in the rat

TitleMechanisms of impaired β-adrenoceptor-induced airway relaxation by interleukin-1β in vivo in the rat
Authors
Issue Date1996
PublisherAmerican Society for Clinical Investigation. The Journal's web site is located at http://www.jci.org
Citation
Journal Of Clinical Investigation, 1996, v. 98 n. 8, p. 1780-1787 How to Cite?
AbstractWe studied the in vivo mechanism of β-adrenergic receptor (β-AR) hyporesponsiveness induced by intratracheal instillation of interleukin-1β (IL-1β, 500 U) in Brown-Norway rats. Tracheal and bronchial smooth muscle responses were measured under isometric conditions ex vivo. Contractile responses to electrical field stimulation and to carbachol were not altered, but maximal relaxation induced by isoproterenol (10-6-10-5 M) was significantly reduced 24 h after IL-1β treatment in tracheal tissues and to a lesser extent, in the main bronchi. Radioligand binding using [125I]iodocyanopindolol revealed a 32±7% reduction in β-ARs in lung tissues from IL-1β-treated rats, without any significant changes in β2-AR mRNA level measured by Northern blot analysis. Autoradiographic studies also showed significant reduction in β2-AR in the airways. Isoproterenol- stimulated cyclic AMP accumulation was reduced by IL-1β at 24 h in trachea and lung tissues. Pertussis toxin reversed this hyporesponsiveness to isoproterenol but not to forskolin in lung tissues. Western blot analysis revealed an IL-1β-induced increase in G(i)α protein expression. Thus, IL- 1β induces an attenuation of β-AR-induced airway relaxation through mechanisms involving a reduction in β-ARs, an increase in G(i)α subunit, and a defect in adenylyl cyclase activity.
Persistent Identifierhttp://hdl.handle.net/10722/162132
ISSN
2015 Impact Factor: 12.575
2015 SCImago Journal Rankings: 8.764
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKoto, Hen_US
dc.contributor.authorMak, JCWen_US
dc.contributor.authorHaddad, EBen_US
dc.contributor.authorXu, WBen_US
dc.contributor.authorSalmon, Men_US
dc.contributor.authorBarnes, PJen_US
dc.contributor.authorChung, KFen_US
dc.date.accessioned2012-09-05T05:17:31Z-
dc.date.available2012-09-05T05:17:31Z-
dc.date.issued1996en_US
dc.identifier.citationJournal Of Clinical Investigation, 1996, v. 98 n. 8, p. 1780-1787en_US
dc.identifier.issn0021-9738en_US
dc.identifier.urihttp://hdl.handle.net/10722/162132-
dc.description.abstractWe studied the in vivo mechanism of β-adrenergic receptor (β-AR) hyporesponsiveness induced by intratracheal instillation of interleukin-1β (IL-1β, 500 U) in Brown-Norway rats. Tracheal and bronchial smooth muscle responses were measured under isometric conditions ex vivo. Contractile responses to electrical field stimulation and to carbachol were not altered, but maximal relaxation induced by isoproterenol (10-6-10-5 M) was significantly reduced 24 h after IL-1β treatment in tracheal tissues and to a lesser extent, in the main bronchi. Radioligand binding using [125I]iodocyanopindolol revealed a 32±7% reduction in β-ARs in lung tissues from IL-1β-treated rats, without any significant changes in β2-AR mRNA level measured by Northern blot analysis. Autoradiographic studies also showed significant reduction in β2-AR in the airways. Isoproterenol- stimulated cyclic AMP accumulation was reduced by IL-1β at 24 h in trachea and lung tissues. Pertussis toxin reversed this hyporesponsiveness to isoproterenol but not to forskolin in lung tissues. Western blot analysis revealed an IL-1β-induced increase in G(i)α protein expression. Thus, IL- 1β induces an attenuation of β-AR-induced airway relaxation through mechanisms involving a reduction in β-ARs, an increase in G(i)α subunit, and a defect in adenylyl cyclase activity.en_US
dc.languageengen_US
dc.publisherAmerican Society for Clinical Investigation. The Journal's web site is located at http://www.jci.orgen_US
dc.relation.ispartofJournal of Clinical Investigationen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAutoradiographyen_US
dc.subject.meshBronchi - Drug Effects - Physiologyen_US
dc.subject.meshCyclic Amp - Metabolismen_US
dc.subject.meshForskolin - Pharmacologyen_US
dc.subject.meshGtp-Binding Proteins - Analysisen_US
dc.subject.meshInterleukin-1 - Pharmacologyen_US
dc.subject.meshIsoproterenol - Pharmacologyen_US
dc.subject.meshMuscle Relaxation - Drug Effectsen_US
dc.subject.meshRna, Messenger - Analysisen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Bnen_US
dc.subject.meshReceptors, Adrenergic, Beta - Analysis - Genetics - Physiologyen_US
dc.subject.meshTrachea - Drug Effects - Physiologyen_US
dc.titleMechanisms of impaired β-adrenoceptor-induced airway relaxation by interleukin-1β in vivo in the raten_US
dc.typeArticleen_US
dc.identifier.emailMak, JCW:judymak@hku.hken_US
dc.identifier.authorityMak, JCW=rp00352en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1172/JCI118977-
dc.identifier.pmid8878428-
dc.identifier.scopuseid_2-s2.0-0029861298en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0029861298&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume98en_US
dc.identifier.issue8en_US
dc.identifier.spage1780en_US
dc.identifier.epage1787en_US
dc.identifier.isiWOS:A1996VN97300013-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKoto, H=7003575947en_US
dc.identifier.scopusauthoridMak, JCW=7103323094en_US
dc.identifier.scopusauthoridHaddad, EB=7102803008en_US
dc.identifier.scopusauthoridXu, WB=36804006100en_US
dc.identifier.scopusauthoridSalmon, M=7102527335en_US
dc.identifier.scopusauthoridBarnes, PJ=36064679400en_US
dc.identifier.scopusauthoridChung, KF=26121035300en_US

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