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Conference Paper: β-Adrenoceptors and the epithelial layer in airways

Titleβ-Adrenoceptors and the epithelial layer in airways
Authors
Issue Date1993
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 1993, v. 52 n. 26, p. 2123-2130 How to Cite?
AbstractAs an inflammatory disorder of the respiratory system, asthma is characterized by bronchial hyper-responsiveness that appears to involve alterations of the bronchial epithelium. The existence of epithelial β-receptors is of particular importance to respiratory function, and epithelial dysfunction in asthma may impair β-adrenoceptor function and lead to bronchial hyper-responsiveness. After reviewing the structure and function of the respiratory epithelium and the role of epithelial β-adrenoceptors, an in vitro model allowing the detailed study of the regulation of airway smooth muscle by epithelial cells is described. Studies with this model have demonstrated that epithelial β-adrenoceptors participate in modulating the tone of bronchial smooth muscle cells. Activation of these β-adrenoceptors leads to bronchial myorelaxation, probably mediated by one or more inhibitory substances generated within the epithelium. In addition, β-adrenoceptor activity may affect smooth muscle tone indirectly by regulating mucociliary clearance and the paracellular exchange of inflammatory mediators. Since some respiratory diseases seem to be associated with β-adrenoceptor dysfunction, therapy with β-agonists may be beneficial by acting on β-adrenoceptors located both on smooth muscle cells and on epithelial cells.
Persistent Identifierhttp://hdl.handle.net/10722/173510
ISSN
2015 Impact Factor: 2.685
2015 SCImago Journal Rankings: 1.056
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMorrison, KJen_US
dc.contributor.authorGao, Yen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:25Z-
dc.date.available2012-10-30T06:32:25Z-
dc.date.issued1993en_US
dc.identifier.citationLife Sciences, 1993, v. 52 n. 26, p. 2123-2130en_US
dc.identifier.issn0024-3205en_US
dc.identifier.urihttp://hdl.handle.net/10722/173510-
dc.description.abstractAs an inflammatory disorder of the respiratory system, asthma is characterized by bronchial hyper-responsiveness that appears to involve alterations of the bronchial epithelium. The existence of epithelial β-receptors is of particular importance to respiratory function, and epithelial dysfunction in asthma may impair β-adrenoceptor function and lead to bronchial hyper-responsiveness. After reviewing the structure and function of the respiratory epithelium and the role of epithelial β-adrenoceptors, an in vitro model allowing the detailed study of the regulation of airway smooth muscle by epithelial cells is described. Studies with this model have demonstrated that epithelial β-adrenoceptors participate in modulating the tone of bronchial smooth muscle cells. Activation of these β-adrenoceptors leads to bronchial myorelaxation, probably mediated by one or more inhibitory substances generated within the epithelium. In addition, β-adrenoceptor activity may affect smooth muscle tone indirectly by regulating mucociliary clearance and the paracellular exchange of inflammatory mediators. Since some respiratory diseases seem to be associated with β-adrenoceptor dysfunction, therapy with β-agonists may be beneficial by acting on β-adrenoceptors located both on smooth muscle cells and on epithelial cells.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescieen_US
dc.relation.ispartofLife Sciencesen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAsthma - Physiopathologyen_US
dc.subject.meshBronchial Hyperreactivity - Physiopathologyen_US
dc.subject.meshEpithelium - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshReceptors, Adrenergic, Beta - Physiologyen_US
dc.subject.meshRespiratory System - Physiopathologyen_US
dc.titleβ-Adrenoceptors and the epithelial layer in airwaysen_US
dc.typeConference_Paperen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/0024-3205(93)90727-Ken_US
dc.identifier.pmid8389954-
dc.identifier.scopuseid_2-s2.0-0027315002en_US
dc.identifier.volume52en_US
dc.identifier.issue26en_US
dc.identifier.spage2123en_US
dc.identifier.epage2130en_US
dc.identifier.isiWOS:A1993LD67700006-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMorrison, KJ=7102484828en_US
dc.identifier.scopusauthoridGao, Y=7404706442en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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