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Article: Products of cyclooxygenase mediate the responses of the guinea pig trachea to hydrogen peroxide

TitleProducts of cyclooxygenase mediate the responses of the guinea pig trachea to hydrogen peroxide
Authors
Issue Date1993
Citation
Journal Of Applied Physiology, 1993, v. 74 n. 5, p. 2105-2111 How to Cite?
AbstractThe role of products of cyclooxygenase was investigated in the responses of isolated airways to H2O2. Strips of guinea pig trachea, in some of which the epithelium had been removed mechanically, were suspended in organ chambers, and isometric tension was recorded. Under basal conditions, H2O2 induced indomethacin-sensitive contractions, which were larger in preparations without than in those with epithelium; the difference was abolished by inhibitors of thromboxane synthase or thromboxane A2 receptors. During contractions to acetylcholine, low concentrations of H2O2 induced relaxation in preparations with but had no significant effect in those without epithelium. At higher concentrations of H2O2, the epithelium- dependent relaxation was attenuated but an epithelium-independent relaxation appeared. The epithelium-dependent but not the epithelium-independent responses to H2O2 were blocked by indomethacin. Under basal conditions, prostaglandin E2 (PGE2; ≤10-7 M), U-46619, prostaglandin PGF(2α) (PGF(2α)), prostaglandin PGD2 (PGD2), and prostacyclin (PGI2) caused contractions. During contractions to acetylcholine, PGE2 induced larger relaxations in preparations with than in those without epithelium. Radioimmunoassay revealed that lower concentrations of H2O2 predominately increased the release of PGE2 and 6-ketoprostaglandin F(1α) (6-keto- PGF(1α)); in preparations without epithelium, the release of thromboxane B2 was augmented also. At higher concentrations of H2O2, the release of PGE2, PGF(2α), PGD2, 6-keto-PGF(1α), and thromboxane B2 increased in preparations with and without epithelium. These findings demonstrate that the responses of the guinea pig trachea to H2O2 are mediated mainly by products of cyclooxygenase and that the effects of H2O2 are modulated by the epithelium.
Persistent Identifierhttp://hdl.handle.net/10722/171087
ISSN
2015 Impact Factor: 3.004
2015 SCImago Journal Rankings: 1.488
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorGao, Yen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:09Z-
dc.date.available2012-10-30T06:12:09Z-
dc.date.issued1993en_US
dc.identifier.citationJournal Of Applied Physiology, 1993, v. 74 n. 5, p. 2105-2111en_US
dc.identifier.issn8750-7587en_US
dc.identifier.urihttp://hdl.handle.net/10722/171087-
dc.description.abstractThe role of products of cyclooxygenase was investigated in the responses of isolated airways to H2O2. Strips of guinea pig trachea, in some of which the epithelium had been removed mechanically, were suspended in organ chambers, and isometric tension was recorded. Under basal conditions, H2O2 induced indomethacin-sensitive contractions, which were larger in preparations without than in those with epithelium; the difference was abolished by inhibitors of thromboxane synthase or thromboxane A2 receptors. During contractions to acetylcholine, low concentrations of H2O2 induced relaxation in preparations with but had no significant effect in those without epithelium. At higher concentrations of H2O2, the epithelium- dependent relaxation was attenuated but an epithelium-independent relaxation appeared. The epithelium-dependent but not the epithelium-independent responses to H2O2 were blocked by indomethacin. Under basal conditions, prostaglandin E2 (PGE2; ≤10-7 M), U-46619, prostaglandin PGF(2α) (PGF(2α)), prostaglandin PGD2 (PGD2), and prostacyclin (PGI2) caused contractions. During contractions to acetylcholine, PGE2 induced larger relaxations in preparations with than in those without epithelium. Radioimmunoassay revealed that lower concentrations of H2O2 predominately increased the release of PGE2 and 6-ketoprostaglandin F(1α) (6-keto- PGF(1α)); in preparations without epithelium, the release of thromboxane B2 was augmented also. At higher concentrations of H2O2, the release of PGE2, PGF(2α), PGD2, 6-keto-PGF(1α), and thromboxane B2 increased in preparations with and without epithelium. These findings demonstrate that the responses of the guinea pig trachea to H2O2 are mediated mainly by products of cyclooxygenase and that the effects of H2O2 are modulated by the epithelium.en_US
dc.languageengen_US
dc.relation.ispartofJournal of Applied Physiologyen_US
dc.subject.mesh15-Hydroxy-11 Alpha,9 Alpha-(Epoxymethano)Prosta-5,13-Dienoic Aciden_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshEpithelium - Physiologyen_US
dc.subject.meshGuinea Pigsen_US
dc.subject.meshHydrazines - Pharmacologyen_US
dc.subject.meshHydrogen Peroxide - Pharmacologyen_US
dc.subject.meshImidazoles - Pharmacologyen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshIsometric Contraction - Drug Effectsen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth - Drug Effects - Enzymologyen_US
dc.subject.meshProstaglandin Endoperoxides, Synthetic - Pharmacologyen_US
dc.subject.meshProstaglandin-Endoperoxide Synthases - Metabolism - Physiologyen_US
dc.subject.meshProstaglandins - Metabolismen_US
dc.subject.meshRadioimmunoassayen_US
dc.subject.meshReceptors, Thromboxane - Antagonists & Inhibitorsen_US
dc.subject.meshThromboxane-A Synthase - Antagonists & Inhibitorsen_US
dc.subject.meshTrachea - Drug Effects - Enzymologyen_US
dc.subject.meshVasoconstrictor Agents - Pharmacologyen_US
dc.titleProducts of cyclooxygenase mediate the responses of the guinea pig trachea to hydrogen peroxideen_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.pmid8335536-
dc.identifier.scopuseid_2-s2.0-0027238916en_US
dc.identifier.volume74en_US
dc.identifier.issue5en_US
dc.identifier.spage2105en_US
dc.identifier.epage2111en_US
dc.identifier.isiWOS:A1993LD69900009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridGao, Y=7404706442en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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