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Article: Short-term exposure to physiological levels of 17β-estradiol enhances endothelium-independent relaxation in porcine coronary artery

TitleShort-term exposure to physiological levels of 17β-estradiol enhances endothelium-independent relaxation in porcine coronary artery
Authors
Issue Date1999
PublisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.org
Citation
Cardiovascular Research, 1999, v. 42 n. 1, p. 224-231 How to Cite?
AbstractObjectives: While alterations in cholesterol and lipoprotein profiles partly account for menopause being a risk factor for coronary heart disease, recent studies have suggested that 17β-estradiol may have vascular effects. Our aims were to study the short-term effects of 17β-estradiol on vascular function in isolated porcine coronary artery rings. Concomitantly, we sought to determine if physiological concentrations of 17β-estradiol could acutely potentiate relaxation. Results: 17α- and 17β-estradiol at pharmacological (>1 μM) concentrations produced relaxation in U46619-pre-contracted porcine coronary artery rings. Relaxation evoked by 17β-estradiol was not reversed by the estrogen receptor antagonists tamoxifen and ICI 182780. Following 20 min exposure to a physiological concentration of 17β-estradiol (1 nM), which on its own had no effect, relaxation elicited by cromakalim, levcromakalim and sodium nitroprusside, but not bradykinin or calcium ionophore A23187, were significantly enhanced. This potentiating action was also insensitive to tamoxifen and ICI 182780. Our data provide evidence for an acute indirect relaxant action of 17β-estradiol and suggest that it may be via a tamoxifen- and ICI 182780-insensitive estrogen receptor. While this response was only observed at pharmacological concentrations, the potentiation of cromakalim, levcromakalim and sodium nitroprusside relaxation was evident in the presence of a physiological concentration (1 nM) of 17β-estradiol. Conclusions: These results demonstrate that short-term exposure to 17β-estradiol, at concentrations that have no effect on their own, can enhance vasorelaxation. These vascular effects may partly account for some of the acute effects of 17β-estradiol on blood flow.
Persistent Identifierhttp://hdl.handle.net/10722/171226
ISSN
2015 Impact Factor: 5.465
2015 SCImago Journal Rankings: 2.897
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTeoh, Hen_US
dc.contributor.authorLeung, SWSen_US
dc.contributor.authorMan, RYKen_US
dc.date.accessioned2012-10-30T06:12:48Z-
dc.date.available2012-10-30T06:12:48Z-
dc.date.issued1999en_US
dc.identifier.citationCardiovascular Research, 1999, v. 42 n. 1, p. 224-231en_US
dc.identifier.issn0008-6363en_US
dc.identifier.urihttp://hdl.handle.net/10722/171226-
dc.description.abstractObjectives: While alterations in cholesterol and lipoprotein profiles partly account for menopause being a risk factor for coronary heart disease, recent studies have suggested that 17β-estradiol may have vascular effects. Our aims were to study the short-term effects of 17β-estradiol on vascular function in isolated porcine coronary artery rings. Concomitantly, we sought to determine if physiological concentrations of 17β-estradiol could acutely potentiate relaxation. Results: 17α- and 17β-estradiol at pharmacological (>1 μM) concentrations produced relaxation in U46619-pre-contracted porcine coronary artery rings. Relaxation evoked by 17β-estradiol was not reversed by the estrogen receptor antagonists tamoxifen and ICI 182780. Following 20 min exposure to a physiological concentration of 17β-estradiol (1 nM), which on its own had no effect, relaxation elicited by cromakalim, levcromakalim and sodium nitroprusside, but not bradykinin or calcium ionophore A23187, were significantly enhanced. This potentiating action was also insensitive to tamoxifen and ICI 182780. Our data provide evidence for an acute indirect relaxant action of 17β-estradiol and suggest that it may be via a tamoxifen- and ICI 182780-insensitive estrogen receptor. While this response was only observed at pharmacological concentrations, the potentiation of cromakalim, levcromakalim and sodium nitroprusside relaxation was evident in the presence of a physiological concentration (1 nM) of 17β-estradiol. Conclusions: These results demonstrate that short-term exposure to 17β-estradiol, at concentrations that have no effect on their own, can enhance vasorelaxation. These vascular effects may partly account for some of the acute effects of 17β-estradiol on blood flow.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.mesh15-Hydroxy-11 Alpha,9 Alpha-(Epoxymethano)Prosta-5,13-Dienoic Acid - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCoronary Vessels - Drug Effectsen_US
dc.subject.meshCromakalim - Pharmacologyen_US
dc.subject.meshDrug Synergismen_US
dc.subject.meshEndothelium, Vascular - Drug Effectsen_US
dc.subject.meshEstradiol - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshEstrogen Antagonists - Pharmacologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshMaleen_US
dc.subject.meshNitroprusside - Pharmacologyen_US
dc.subject.meshSwineen_US
dc.subject.meshTamoxifen - Pharmacologyen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshVasoconstrictor Agents - Pharmacologyen_US
dc.subject.meshVasodilation - Drug Effectsen_US
dc.titleShort-term exposure to physiological levels of 17β-estradiol enhances endothelium-independent relaxation in porcine coronary arteryen_US
dc.typeArticleen_US
dc.identifier.emailLeung, SWS:swsleung@hku.hken_US
dc.identifier.emailMan, RYK:rykman@hkucc.hku.hken_US
dc.identifier.authorityLeung, SWS=rp00235en_US
dc.identifier.authorityMan, RYK=rp00236en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0008-6363(98)00265-Xen_US
dc.identifier.pmid10435014-
dc.identifier.scopuseid_2-s2.0-0032941614en_US
dc.identifier.hkuros41192-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032941614&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume42en_US
dc.identifier.issue1en_US
dc.identifier.spage224en_US
dc.identifier.epage231en_US
dc.identifier.isiWOS:000079645300028-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridTeoh, H=7003816542en_US
dc.identifier.scopusauthoridLeung, SWS=24540419500en_US
dc.identifier.scopusauthoridMan, RYK=7004986435en_US

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