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Article: Nickel inhibits urocortin-induced relaxation in the rat pulmonary artery

TitleNickel inhibits urocortin-induced relaxation in the rat pulmonary artery
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2004
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejphar
Citation
European Journal Of Pharmacology, 2004, v. 488 n. 1-3, p. 169-172 How to Cite?
AbstractUrocortin relaxes rat pulmonary arteries partly through a cyclic AMP-dependent but Ca2+ channel-independent mechanism. However, other participating mechanisms are relatively unknown. The present study was designed to examine whether the forward mode of Na+-Ca2+ exchangers play a role in the relaxant responses to urocortin in isolated rat small pulmonary arteries. Endothelium-denuded rings were mounted on small vessel myographs for measurement of changes in isometric tension. Urocortin inhibited 9,11-dideoxy-11α,9α-epoxy-methanoprostaglandin F 2α (U46619)-induced contraction in a concentration-dependent manner and this inhibition was reversed by astressin, a corticotropin-releasing factor receptor antagonist. Micromolar concentrations of nickel (Ni 2+) chloride, a putative inhibitor of the Na+-Ca 2+ exchanger, reduced the relaxant responses to urocortin. Urocortin-induced relaxation was abolished in a Na+-free solution, a condition that eliminates influence of the forward mode of Na +-Ca2+ exchanger. In contrast, the relaxant responses to atrial natriuretic peptide or forskolin were unaffected by Ni2+ or with removal of extracellular Na+. The present results provide indirect evidence suggesting that stimulation of Na+-Ca2+ exchangers may contribute to urocortin-induced endothelium-independent pulmonary artery relaxation. © 2004 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/134684
ISSN
2015 Impact Factor: 2.73
2015 SCImago Journal Rankings: 1.115
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLau, CWen_HK
dc.contributor.authorChan, YCen_HK
dc.contributor.authorYao, Xen_HK
dc.contributor.authorChan, FLen_HK
dc.contributor.authorChen, ZYen_HK
dc.contributor.authorHuang, Yuen_HK
dc.date.accessioned2011-07-05T08:24:20Z-
dc.date.available2011-07-05T08:24:20Z-
dc.date.issued2004en_HK
dc.identifier.citationEuropean Journal Of Pharmacology, 2004, v. 488 n. 1-3, p. 169-172en_HK
dc.identifier.issn0014-2999en_HK
dc.identifier.urihttp://hdl.handle.net/10722/134684-
dc.description.abstractUrocortin relaxes rat pulmonary arteries partly through a cyclic AMP-dependent but Ca2+ channel-independent mechanism. However, other participating mechanisms are relatively unknown. The present study was designed to examine whether the forward mode of Na+-Ca2+ exchangers play a role in the relaxant responses to urocortin in isolated rat small pulmonary arteries. Endothelium-denuded rings were mounted on small vessel myographs for measurement of changes in isometric tension. Urocortin inhibited 9,11-dideoxy-11α,9α-epoxy-methanoprostaglandin F 2α (U46619)-induced contraction in a concentration-dependent manner and this inhibition was reversed by astressin, a corticotropin-releasing factor receptor antagonist. Micromolar concentrations of nickel (Ni 2+) chloride, a putative inhibitor of the Na+-Ca 2+ exchanger, reduced the relaxant responses to urocortin. Urocortin-induced relaxation was abolished in a Na+-free solution, a condition that eliminates influence of the forward mode of Na +-Ca2+ exchanger. In contrast, the relaxant responses to atrial natriuretic peptide or forskolin were unaffected by Ni2+ or with removal of extracellular Na+. The present results provide indirect evidence suggesting that stimulation of Na+-Ca2+ exchangers may contribute to urocortin-induced endothelium-independent pulmonary artery relaxation. © 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/ejpharen_HK
dc.relation.ispartofEuropean Journal of Pharmacologyen_HK
dc.subjectChemicals And Cas Registry Numbersen_US
dc.subject.mesh15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - pharmacologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAtrial Natriuretic Factor - pharmacologyen_HK
dc.subject.meshCorticotropin-Releasing Hormone - antagonists & inhibitors - pharmacologyen_HK
dc.subject.meshForskolin - pharmacologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMuscle Contraction - drug effectsen_HK
dc.subject.meshMuscle Relaxation - drug effectsen_HK
dc.subject.meshMuscle, Smooth, Vascular - drug effectsen_HK
dc.subject.meshNickel - pharmacologyen_HK
dc.subject.meshPotassium - pharmacologyen_HK
dc.subject.meshPulmonary Artery - drug effectsen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshSodium-Calcium Exchanger - antagonists & inhibitorsen_HK
dc.subject.meshUrocortinsen_HK
dc.subject.meshVasoconstrictor Agents - pharmacologyen_HK
dc.titleNickel inhibits urocortin-induced relaxation in the rat pulmonary arteryen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, YC:yauchi@graduate.hku.hken_HK
dc.identifier.authorityChan, YC=rp01502en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.ejphar.2004.01.024en_HK
dc.identifier.pmid15044048-
dc.identifier.scopuseid_2-s2.0-1642278590en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1642278590&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume488en_HK
dc.identifier.issue1-3en_HK
dc.identifier.spage169en_HK
dc.identifier.epage172en_HK
dc.identifier.isiWOS:000220692000020-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridLau, CW=7401968520en_HK
dc.identifier.scopusauthoridChan, YC=7403676116en_HK
dc.identifier.scopusauthoridYao, X=7402529434en_HK
dc.identifier.scopusauthoridChan, FL=15050111400en_HK
dc.identifier.scopusauthoridChen, ZY=7409487061en_HK
dc.identifier.scopusauthoridHuang, Yu=7501573013en_HK

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