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Article: Acute impairment of contractile responses by 17β-estradiol is cAMP and protein kinase G dependent in vascular smooth muscle cells of the porcine coronary arteries

TitleAcute impairment of contractile responses by 17β-estradiol is cAMP and protein kinase G dependent in vascular smooth muscle cells of the porcine coronary arteries
Authors
Keywords17β-estradiol
CAMP
CAMP-dependent protein kinase
CGMP
CGMP-dependent protein kinase, porcine coronary artery
Isoproterenol
Vascular smooth muscle
Issue Date2005
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 2005, v. 144 n. 1, p. 71-79 How to Cite?
Abstract1 The aim of the present study was to investigate the involvement of adenosine 3′, 5′-cyclic monophosphate (cAMP) cascade in the acute impairment of contraction by 17β-estradiol in porcine coronary arteries, and to elucidate the signaling pathway leading to the activation of this cascade by the hormone. 2 Isometric tension was recorded in isolated rings of porcine coronary arteries. 3 The contraction to U46619 was reduced significantly following 30 min incubation with 1 nM 17β-estradiol or 1 nM isoproterenol. There was no additive effect when 17β-estradiol and isoproterenol were administered together. The effect of 17β-estradiol was mimicked by both the cyclic AMP analogue 8-Br-cAMP and the guanosine 3′,5′-cyclic monophosphate (cyclic GMP) analogue 8-Br-cGMP. 4 In rings with and without endothelium, the modulatory effect of 17β-estradiol was abolished by the adenylyl cyclase inhibitor, SQ 22536, but was unaffected by the guanylyl cyclase inhibitor, ODQ. 5 Both the cAMP antagonist Rp-8-Br-cAMPS and the cGMP antagonist inhibitor Rp-8-Br-cGMPS inhibited the effect of 17β-estradiol. 6 The effect of 17β-estradiol was unaffected by the protein kinase A inhibitor, KT5720, but was abolished by the protein kinase G (PKG) inhibitor, KT5823, which also abolished the effect of isoproterenol. 7 These data support our earlier findings that 17β-estradiol (1nM) acutely impairs contractile responses of porcine coronary arteries in vitro. This acute effect of 17β-estradiol involves cAMP in vascular smooth muscles and the activation of PKG.
Persistent Identifierhttp://hdl.handle.net/10722/49281
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKeung, Wen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorMan, RYKen_HK
dc.date.accessioned2008-06-12T06:38:24Z-
dc.date.available2008-06-12T06:38:24Z-
dc.date.issued2005en_HK
dc.identifier.citationBritish Journal Of Pharmacology, 2005, v. 144 n. 1, p. 71-79en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49281-
dc.description.abstract1 The aim of the present study was to investigate the involvement of adenosine 3′, 5′-cyclic monophosphate (cAMP) cascade in the acute impairment of contraction by 17β-estradiol in porcine coronary arteries, and to elucidate the signaling pathway leading to the activation of this cascade by the hormone. 2 Isometric tension was recorded in isolated rings of porcine coronary arteries. 3 The contraction to U46619 was reduced significantly following 30 min incubation with 1 nM 17β-estradiol or 1 nM isoproterenol. There was no additive effect when 17β-estradiol and isoproterenol were administered together. The effect of 17β-estradiol was mimicked by both the cyclic AMP analogue 8-Br-cAMP and the guanosine 3′,5′-cyclic monophosphate (cyclic GMP) analogue 8-Br-cGMP. 4 In rings with and without endothelium, the modulatory effect of 17β-estradiol was abolished by the adenylyl cyclase inhibitor, SQ 22536, but was unaffected by the guanylyl cyclase inhibitor, ODQ. 5 Both the cAMP antagonist Rp-8-Br-cAMPS and the cGMP antagonist inhibitor Rp-8-Br-cGMPS inhibited the effect of 17β-estradiol. 6 The effect of 17β-estradiol was unaffected by the protein kinase A inhibitor, KT5720, but was abolished by the protein kinase G (PKG) inhibitor, KT5823, which also abolished the effect of isoproterenol. 7 These data support our earlier findings that 17β-estradiol (1nM) acutely impairs contractile responses of porcine coronary arteries in vitro. This acute effect of 17β-estradiol involves cAMP in vascular smooth muscles and the activation of PKG.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_HK
dc.relation.ispartofBritish Journal of Pharmacologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject17β-estradiolen_HK
dc.subjectCAMPen_HK
dc.subjectCAMP-dependent protein kinaseen_HK
dc.subjectCGMPen_HK
dc.subjectCGMP-dependent protein kinase, porcine coronary arteryen_HK
dc.subjectIsoproterenolen_HK
dc.subjectVascular smooth muscleen_HK
dc.titleAcute impairment of contractile responses by 17β-estradiol is cAMP and protein kinase G dependent in vascular smooth muscle cells of the porcine coronary arteriesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-1188&volume=144&issue=1&spage=71&epage=79&date=2005&atitle=Acute+impairment+of+contractile+responses+by+17β-estradiol+is+cAMP+and+protein+kinase+G+dependent+in+vascular+smooth+muscle+cells+of+the+porcine+coronary+arteriesen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1038/sj.bjp.0706018en_HK
dc.identifier.pmid15644870-
dc.identifier.pmcidPMC1575973en_HK
dc.identifier.scopuseid_2-s2.0-13244255269en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-13244255269&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume144en_HK
dc.identifier.issue1en_HK
dc.identifier.spage71en_HK
dc.identifier.epage79en_HK
dc.identifier.isiWOS:000226645300009-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridKeung, W=19337708900en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridMan, RYK=7004986435en_HK

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