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Article: The relaxant effect of urocortin in rat pulmonary arteries

TitleThe relaxant effect of urocortin in rat pulmonary arteries
Authors
KeywordsPulmonary arteries
Rats
Relaxation
Urocortin
Issue Date2004
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/regpep
Citation
Regulatory Peptides, 2004, v. 121 n. 1-3, p. 11-18 How to Cite?
AbstractUrocortin is a potent vasodilator, which plays physiological or pathophysiological roles in systemic circulation. However, little is known about its action on pulmonary circulation. The present study was aimed to characterize some cellular mechanisms underlying the relaxant effect of urocortin in isolated rat pulmonary arteries. Changes in isometric tension were measured on small vessel myographs. Urocortin inhibited U46619-induced contraction with reduction of the maximal response. Urocortin-induced relaxation was independent of the presence of endothelium. Inhibitors of nitric oxide (NO)-dependent dilator, NG-nitro-L-arginine methyl ester or 1H-[1,2,4]oxadizolo[4,3-a]quinoxalin-1-one, did not affect the relaxation. Astressin (100-500 nM), a corticotropin-releasing factor (CRF) receptor antagonist and KT5720, a protein kinase A (PKA) inhibitor reduced urocortin-induced relaxation. Urocortin produced less relaxant effect in 30 mM K+- than U46619-contracted arterial rings. Urocortin did not reduce CaCl2-induced contraction in 60 mM K+-containing solution. Ba2+ (100-500 μM) but not other K+ channel blockers reduced the relaxant responses to urocortin. Urocortin also relaxed the rings preconstricted by phorbol 12,13-diacetae in normal Krebs solution while this relaxation was less in a Ca2+-free solution. Our results show that urocortin relaxed rat pulmonary arteries via CRF receptor-mediated and PKA-dependent but endothelium/NO or voltage-gated Ca2+ channel-independent mechanisms. Stimulation of Ba2+-sensitive K + channel may contribute to urocortin-induced relaxation. Finally, urocortin relaxed pulmonary arteries partly via inhibition of a PKC-dependent contractile mechanism. © 2004 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/134683
ISSN
2015 Impact Factor: 1.813
2015 SCImago Journal Rankings: 0.915
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, YCen_HK
dc.contributor.authorYao, XQen_HK
dc.contributor.authorLau, CWen_HK
dc.contributor.authorChan, FLen_HK
dc.contributor.authorHe, GWen_HK
dc.contributor.authorBourreau, JPen_HK
dc.contributor.authorHuang, Yen_HK
dc.date.accessioned2011-07-05T08:24:19Z-
dc.date.available2011-07-05T08:24:19Z-
dc.date.issued2004en_HK
dc.identifier.citationRegulatory Peptides, 2004, v. 121 n. 1-3, p. 11-18en_HK
dc.identifier.issn0167-0115en_HK
dc.identifier.urihttp://hdl.handle.net/10722/134683-
dc.description.abstractUrocortin is a potent vasodilator, which plays physiological or pathophysiological roles in systemic circulation. However, little is known about its action on pulmonary circulation. The present study was aimed to characterize some cellular mechanisms underlying the relaxant effect of urocortin in isolated rat pulmonary arteries. Changes in isometric tension were measured on small vessel myographs. Urocortin inhibited U46619-induced contraction with reduction of the maximal response. Urocortin-induced relaxation was independent of the presence of endothelium. Inhibitors of nitric oxide (NO)-dependent dilator, NG-nitro-L-arginine methyl ester or 1H-[1,2,4]oxadizolo[4,3-a]quinoxalin-1-one, did not affect the relaxation. Astressin (100-500 nM), a corticotropin-releasing factor (CRF) receptor antagonist and KT5720, a protein kinase A (PKA) inhibitor reduced urocortin-induced relaxation. Urocortin produced less relaxant effect in 30 mM K+- than U46619-contracted arterial rings. Urocortin did not reduce CaCl2-induced contraction in 60 mM K+-containing solution. Ba2+ (100-500 μM) but not other K+ channel blockers reduced the relaxant responses to urocortin. Urocortin also relaxed the rings preconstricted by phorbol 12,13-diacetae in normal Krebs solution while this relaxation was less in a Ca2+-free solution. Our results show that urocortin relaxed rat pulmonary arteries via CRF receptor-mediated and PKA-dependent but endothelium/NO or voltage-gated Ca2+ channel-independent mechanisms. Stimulation of Ba2+-sensitive K + channel may contribute to urocortin-induced relaxation. Finally, urocortin relaxed pulmonary arteries partly via inhibition of a PKC-dependent contractile mechanism. © 2004 Elsevier B.V. All rights reserved.en_HK
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/regpepen_HK
dc.relation.ispartofRegulatory Peptidesen_HK
dc.rightsRegulatory Peptides. Copyright © Elsevier BV.-
dc.subjectPulmonary arteries-
dc.subjectRats-
dc.subjectRelaxation-
dc.subjectUrocortin-
dc.subject.meshAnimalsen_HK
dc.subject.meshBarium Compounds - pharmacologyen_HK
dc.subject.meshCarbazoles - pharmacologyen_HK
dc.subject.meshChlorides - pharmacologyen_HK
dc.subject.meshCorticotropin-Releasing Hormone - antagonists & inhibitors - metabolism - pharmacologyen_HK
dc.subject.meshEndothelium - drug effects - enzymology - metabolismen_HK
dc.subject.meshIndoles - pharmacologyen_HK
dc.subject.meshMuscle Relaxation - drug effectsen_HK
dc.subject.meshNitric Oxide - antagonists & inhibitors - metabolismen_HK
dc.subject.meshPotassium Channel Blockers - pharmacologyen_HK
dc.subject.meshPotassium Channels - metabolismen_HK
dc.subject.meshProtein Kinase C - antagonists & inhibitors - metabolismen_HK
dc.subject.meshPulmonary Artery - drug effects - physiologyen_HK
dc.subject.meshPyrroles - pharmacologyen_HK
dc.subject.meshRatsen_HK
dc.subject.meshUrocortinsen_HK
dc.titleThe relaxant effect of urocortin in rat pulmonary arteriesen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, YC:yauchi@graduate.hku.hken_HK
dc.identifier.emailBourreau, JP:bourreau@hkucc.hku.hken_HK
dc.identifier.authorityChan, YC=rp01502en_HK
dc.identifier.authorityBourreau, JP=rp00389en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.regpep.2004.03.019en_HK
dc.identifier.pmid15256268-
dc.identifier.scopuseid_2-s2.0-1642396172en_HK
dc.identifier.hkuros95652-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1642396172&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume121en_HK
dc.identifier.issue1-3en_HK
dc.identifier.spage11en_HK
dc.identifier.epage18en_HK
dc.identifier.isiWOS:000222925200002-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridChan, YC=7403676116en_HK
dc.identifier.scopusauthoridYao, XQ=7402529434en_HK
dc.identifier.scopusauthoridLau, CW=7401968520en_HK
dc.identifier.scopusauthoridChan, FL=15050111400en_HK
dc.identifier.scopusauthoridHe, GW=7401955801en_HK
dc.identifier.scopusauthoridBourreau, JP=7003927886en_HK
dc.identifier.scopusauthoridHuang, Y=7501573013en_HK

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