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Article: Isoproterenol amplifies 17β-estradiol-mediated vasorelaxation: Role of endothelium/nitric oxide and cyclic AMP

TitleIsoproterenol amplifies 17β-estradiol-mediated vasorelaxation: Role of endothelium/nitric oxide and cyclic AMP
Authors
Issue Date2002
PublisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.org
Citation
Cardiovascular Research, 2002, v. 53 n. 3, p. 627-633 How to Cite?
AbstractObjectives: Estrogen exerts cardiac protection via multiple cellular mechanisms. Estrogen modifies vasodilatation induced by certain relaxants such as β-adrenoceptor agonists. However, little is known whether low concentrations of β-adrenoceptor agonists would reciprocally influence the acute relaxant response to estrogen. The present study was designed to investigate the synergistic interaction between isoproterenol and 17β-estradiol, and the role of endothelium and cyclic AMP-dependent pathway in this interaction. Methods: Changes in vessel tone of the isolated rat mesenteric artery rings were measured using a force-displacement Grass transducer. Results: In 9,11-dideoxy-11α, 9α-epoxy-methanoprostaglandin F 2α-preconstricted endothelium-intact rings, 17β-estradiol induced relaxations with pD 2 of 5.06±0.06. Pretreatment of endothelium-intact rings with isoproterenol (1-3×10 -9 M, 1 h incubation time) significantly enhanced 17β-estradiol-induced relaxation. This effect was inhibited by Rp-cGMPS triethylamine (3×10 -6 M), and abolished in the presence of 3×10 -5 M N G-nitro-L-arginine methyl ester or in endothelium-denuded rings. The effect of isoproterenol was antagonized by propranolol (3×10 -6 M), ICI 118,551 (3×10 -6 M), but not by atenolol (10 -5 M). Rp-cAMPS triethylamine (3×10 -6 M) abolished the effect of isoproterenol. Besides, exposure to 3×10 -9 M forskolin for 1 h also potentiated the relaxant response to 17β-estradiol. Conclusion: In endothelium-intact rat mesenteric arteries pretreatment with low concentrations of isoproterenol enhanced the acute relaxant response to 17β-estradiol. This enhancement was dependent on the presence of endothelium and abolished by L-NAME via a β 2-adrenoceptor-mediated cyclic AMP-dependent mechanism. © 2002 Elsevier Science B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/171709
ISSN
2015 Impact Factor: 5.465
2015 SCImago Journal Rankings: 2.897
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, HYen_US
dc.contributor.authorYao, Xen_US
dc.contributor.authorTsang, SYen_US
dc.contributor.authorBourreau, JPen_US
dc.contributor.authorChan, FLen_US
dc.contributor.authorHuang, Yen_US
dc.date.accessioned2012-10-30T06:16:32Z-
dc.date.available2012-10-30T06:16:32Z-
dc.date.issued2002en_US
dc.identifier.citationCardiovascular Research, 2002, v. 53 n. 3, p. 627-633en_US
dc.identifier.issn0008-6363en_US
dc.identifier.urihttp://hdl.handle.net/10722/171709-
dc.description.abstractObjectives: Estrogen exerts cardiac protection via multiple cellular mechanisms. Estrogen modifies vasodilatation induced by certain relaxants such as β-adrenoceptor agonists. However, little is known whether low concentrations of β-adrenoceptor agonists would reciprocally influence the acute relaxant response to estrogen. The present study was designed to investigate the synergistic interaction between isoproterenol and 17β-estradiol, and the role of endothelium and cyclic AMP-dependent pathway in this interaction. Methods: Changes in vessel tone of the isolated rat mesenteric artery rings were measured using a force-displacement Grass transducer. Results: In 9,11-dideoxy-11α, 9α-epoxy-methanoprostaglandin F 2α-preconstricted endothelium-intact rings, 17β-estradiol induced relaxations with pD 2 of 5.06±0.06. Pretreatment of endothelium-intact rings with isoproterenol (1-3×10 -9 M, 1 h incubation time) significantly enhanced 17β-estradiol-induced relaxation. This effect was inhibited by Rp-cGMPS triethylamine (3×10 -6 M), and abolished in the presence of 3×10 -5 M N G-nitro-L-arginine methyl ester or in endothelium-denuded rings. The effect of isoproterenol was antagonized by propranolol (3×10 -6 M), ICI 118,551 (3×10 -6 M), but not by atenolol (10 -5 M). Rp-cAMPS triethylamine (3×10 -6 M) abolished the effect of isoproterenol. Besides, exposure to 3×10 -9 M forskolin for 1 h also potentiated the relaxant response to 17β-estradiol. Conclusion: In endothelium-intact rat mesenteric arteries pretreatment with low concentrations of isoproterenol enhanced the acute relaxant response to 17β-estradiol. This enhancement was dependent on the presence of endothelium and abolished by L-NAME via a β 2-adrenoceptor-mediated cyclic AMP-dependent mechanism. © 2002 Elsevier Science B.V. All rights reserved.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.orgen_US
dc.relation.ispartofCardiovascular Researchen_US
dc.rightsCardiovascular Research. Copyright © Elsevier BV.-
dc.subject.meshAdrenergic Beta-Agonists - Pharmacologyen_US
dc.subject.meshAdrenergic Beta-Antagonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAtenolol - Pharmacologyen_US
dc.subject.meshCyclic Amp - Metabolismen_US
dc.subject.meshDrug Synergismen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Metabolismen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshEstradiol - Pharmacologyen_US
dc.subject.meshIsoproterenol - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMesenteric Arteriesen_US
dc.subject.meshNg-Nitroarginine Methyl Ester - Pharmacologyen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshNitric Oxide Synthase - Antagonists & Inhibitorsen_US
dc.subject.meshPropanolamines - Pharmacologyen_US
dc.subject.meshPropranolol - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshVasodilation - Drug Effectsen_US
dc.titleIsoproterenol amplifies 17β-estradiol-mediated vasorelaxation: Role of endothelium/nitric oxide and cyclic AMPen_US
dc.typeArticleen_US
dc.identifier.emailBourreau, JP:bourreau@hkucc.hku.hken_US
dc.identifier.authorityBourreau, JP=rp00389en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0008-6363(01)00498-9en_US
dc.identifier.pmid11861033-
dc.identifier.scopuseid_2-s2.0-0037083820en_US
dc.identifier.hkuros82112-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037083820&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume53en_US
dc.identifier.issue3en_US
dc.identifier.spage627en_US
dc.identifier.epage633en_US
dc.identifier.isiWOS:000174980700011-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridChan, HY=7403402342en_US
dc.identifier.scopusauthoridYao, X=7402529434en_US
dc.identifier.scopusauthoridTsang, SY=7102255908en_US
dc.identifier.scopusauthoridBourreau, JP=7003927886en_US
dc.identifier.scopusauthoridChan, FL=15050111400en_US
dc.identifier.scopusauthoridHuang, Y=7501573013en_US

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