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Article: Tachykinin control of ferret airways: Mucus secretion, bronchoconstriction and receptor mapping

TitleTachykinin control of ferret airways: Mucus secretion, bronchoconstriction and receptor mapping
Authors
Issue Date1993
PublisherChurchill Livingstone. The Journal's web site is located at http://www.elsevier.com/locate/npep
Citation
Neuropeptides, 1993, v. 24 n. 2, p. 81-89 How to Cite?
AbstractThe effects of synthetic tachykinin receptor agonists on mucus secretion by ferret trachea was determined in vitro in Ussing chambers using 35SO4 as a mucus marker and the synthetic peptides [Sar9,Met(O2)11]substance P (SarSP), [βAla8]neurokinin A-(4-10) and [MePhe7] neurokinin B which are selective for NK1, NK2 and NK3 tachykinin-receptors respectively. The bronchomotor effects of the same agonists were also studied in vitro and tachykinin receptors were localized by autoradiographic mapping. SarSP was the only synthetic agonist able to elicit a concentration-dependent increase in mucus secretion and was much more potent than SP. The EC50 for SarSP was 1.7 x 10-6 M. Moreover, the maximal increase in release of 35SO4 produced by SarSP 10-5 M was 95% of the increase produced by methacholine 10-4 M indicating that this concentration of SarSP induced a near maximal secretory response. There was no significant difference in the secretory action of SP administered from the luminal or the submucosal side of the tissue. Only the NK2 agonist was able to produce a concentration-dependent contractility of bronchial ring preparations and its effect was relatively weak (EC50 6.4 x 10-6 M). Capsaicin (10-5 M) produced only a slight increase in tracheal mucus secretion (28 ± 5%; n = 6) and was completely ineffective in inducing bronchoconstriction. Binding sites for [125I]-Bolton Hunter SP were more evident than sites for [125I]-NKA on submucosal glands and epithelium. In contrast, only binding sites to NKA could be observed over the smooth muscle. We conclude that in ferret trachea activation of NK1 receptors is able to elicit output of 35SO4-labelled mucins whilst activation of NK2 or NK3 receptors does not. The bronchomotor response seems to be dependent on the activation of NK2 receptors.
Persistent Identifierhttp://hdl.handle.net/10722/162011
ISSN
2015 Impact Factor: 2.726
2015 SCImago Journal Rankings: 1.165
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMeini, Sen_US
dc.contributor.authorMak, JCWen_US
dc.contributor.authorRohde, JALen_US
dc.contributor.authorRogers, DFen_US
dc.date.accessioned2012-09-05T05:16:40Z-
dc.date.available2012-09-05T05:16:40Z-
dc.date.issued1993en_US
dc.identifier.citationNeuropeptides, 1993, v. 24 n. 2, p. 81-89en_US
dc.identifier.issn0143-4179en_US
dc.identifier.urihttp://hdl.handle.net/10722/162011-
dc.description.abstractThe effects of synthetic tachykinin receptor agonists on mucus secretion by ferret trachea was determined in vitro in Ussing chambers using 35SO4 as a mucus marker and the synthetic peptides [Sar9,Met(O2)11]substance P (SarSP), [βAla8]neurokinin A-(4-10) and [MePhe7] neurokinin B which are selective for NK1, NK2 and NK3 tachykinin-receptors respectively. The bronchomotor effects of the same agonists were also studied in vitro and tachykinin receptors were localized by autoradiographic mapping. SarSP was the only synthetic agonist able to elicit a concentration-dependent increase in mucus secretion and was much more potent than SP. The EC50 for SarSP was 1.7 x 10-6 M. Moreover, the maximal increase in release of 35SO4 produced by SarSP 10-5 M was 95% of the increase produced by methacholine 10-4 M indicating that this concentration of SarSP induced a near maximal secretory response. There was no significant difference in the secretory action of SP administered from the luminal or the submucosal side of the tissue. Only the NK2 agonist was able to produce a concentration-dependent contractility of bronchial ring preparations and its effect was relatively weak (EC50 6.4 x 10-6 M). Capsaicin (10-5 M) produced only a slight increase in tracheal mucus secretion (28 ± 5%; n = 6) and was completely ineffective in inducing bronchoconstriction. Binding sites for [125I]-Bolton Hunter SP were more evident than sites for [125I]-NKA on submucosal glands and epithelium. In contrast, only binding sites to NKA could be observed over the smooth muscle. We conclude that in ferret trachea activation of NK1 receptors is able to elicit output of 35SO4-labelled mucins whilst activation of NK2 or NK3 receptors does not. The bronchomotor response seems to be dependent on the activation of NK2 receptors.en_US
dc.languageengen_US
dc.publisherChurchill Livingstone. The Journal's web site is located at http://www.elsevier.com/locate/npepen_US
dc.relation.ispartofNeuropeptidesen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBronchoconstriction - Drug Effectsen_US
dc.subject.meshCapsaicin - Pharmacologyen_US
dc.subject.meshFerretsen_US
dc.subject.meshMaleen_US
dc.subject.meshMethacholine Chloride - Pharmacologyen_US
dc.subject.meshMucus - Secretionen_US
dc.subject.meshMuscle, Smooth - Drug Effectsen_US
dc.subject.meshNeurokinin A - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshNeurokinin B - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshPeptide Fragments - Pharmacologyen_US
dc.subject.meshReceptors, Neurotransmitter - Drug Effects - Physiologyen_US
dc.subject.meshReceptors, Tachykininen_US
dc.subject.meshReproducibility Of Resultsen_US
dc.subject.meshStimulation, Chemicalen_US
dc.subject.meshSubstance P - Administration & Dosage - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshTachykinins - Physiologyen_US
dc.subject.meshTrachea - Drug Effects - Secretionen_US
dc.titleTachykinin control of ferret airways: Mucus secretion, bronchoconstriction and receptor mappingen_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.doi10.1016/0143-4179(93)90025-6en_US
dc.identifier.pmid7681552-
dc.identifier.scopuseid_2-s2.0-0027533460en_US
dc.identifier.volume24en_US
dc.identifier.issue2en_US
dc.identifier.spage81en_US
dc.identifier.epage89en_US
dc.identifier.isiWOS:A1993KN34300003-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridMeini, S=7003356985en_US
dc.identifier.scopusauthoridMak, JCW=7103323094en_US
dc.identifier.scopusauthoridRohde, JAL=7102243322en_US
dc.identifier.scopusauthoridRogers, DF=7402049007en_US

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