File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Non-genomic activation of adenylyl cyclase and protein kinase G by 17β-estradiol in vascular smooth muscle of the rat superior mesenteric artery

TitleNon-genomic activation of adenylyl cyclase and protein kinase G by 17β-estradiol in vascular smooth muscle of the rat superior mesenteric artery
Authors
KeywordscAMP
Caveolae
Estrogen
Non-genomic effects
PKG
Vascular smooth muscle
Issue Date2011
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/issn/10436618
Citation
Pharmacological Research, 2011, v. 64 n. 5, p. 509-516 How to Cite?
AbstractThe aim of the present study was to investigate the signaling mechanisms underlying the non-genomic effects of estrogen in rat superior mesenteric arteries. Isometric tension was recorded in rings with or without endothelium. Changes in cyclic nucleotide levels and protein kinase (PK) activities were measured. Localization of estrogen receptors (ER) and caveolin-1 were visualized by confocal microscopy. 17β-Estradiol elicited a concentration-dependent relaxation. The relaxation was reduced by SQ 22536 (adenylyl cyclase inhibitor) and KT 5823 (PKG inhibitor) while ODQ (guanylyl cyclase inhibitor) and KT 5720 (PKA inhibitor) had no effect. At the physiological concentration of 1 nM, 17β-estradiol had no significant effect on relaxation but enhanced the relaxation to sodium nitroprusside. The enhancement of relaxation by 17β-estradiol was blocked by SQ 22536 and KT 5823. Although 1 nM 17β-estradiol or 10 nM sodium nitroprusside given alone had minimal effects on PKG activity, in their combined presence, a significant increase in PKG activity was observed. Confocal microscopy demonstrated that ERα and ERβ colocalized with caveolin-1 and PKG in vascular smooth muscle cells. The present findings suggest that 17β-estradiol enhances relaxation of vascular smooth muscle of the rat superior mesenteric artery by activating adenylyl cyclase, leading to an increase in cAMP which cross activates PKG in the caveolae. No detectable increase in total cAMP level was detected as these changes occurred in the caveolae. These results are consistent with the notion that 17β-estradiol mediates its effect in the distinct microdomains of the caveolae of the plasma membrane with colocalization of adenylyl cyclase and PKG. © 2011 Elsevier Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/152759
ISSN
2015 Impact Factor: 4.816
2015 SCImago Journal Rankings: 2.108
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKeung, Wen_HK
dc.contributor.authorChan, MLYen_HK
dc.contributor.authorHo, EYWen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorMan, RYKen_HK
dc.date.accessioned2012-07-16T09:47:35Z-
dc.date.available2012-07-16T09:47:35Z-
dc.date.issued2011en_HK
dc.identifier.citationPharmacological Research, 2011, v. 64 n. 5, p. 509-516en_HK
dc.identifier.issn1043-6618en_HK
dc.identifier.urihttp://hdl.handle.net/10722/152759-
dc.description.abstractThe aim of the present study was to investigate the signaling mechanisms underlying the non-genomic effects of estrogen in rat superior mesenteric arteries. Isometric tension was recorded in rings with or without endothelium. Changes in cyclic nucleotide levels and protein kinase (PK) activities were measured. Localization of estrogen receptors (ER) and caveolin-1 were visualized by confocal microscopy. 17β-Estradiol elicited a concentration-dependent relaxation. The relaxation was reduced by SQ 22536 (adenylyl cyclase inhibitor) and KT 5823 (PKG inhibitor) while ODQ (guanylyl cyclase inhibitor) and KT 5720 (PKA inhibitor) had no effect. At the physiological concentration of 1 nM, 17β-estradiol had no significant effect on relaxation but enhanced the relaxation to sodium nitroprusside. The enhancement of relaxation by 17β-estradiol was blocked by SQ 22536 and KT 5823. Although 1 nM 17β-estradiol or 10 nM sodium nitroprusside given alone had minimal effects on PKG activity, in their combined presence, a significant increase in PKG activity was observed. Confocal microscopy demonstrated that ERα and ERβ colocalized with caveolin-1 and PKG in vascular smooth muscle cells. The present findings suggest that 17β-estradiol enhances relaxation of vascular smooth muscle of the rat superior mesenteric artery by activating adenylyl cyclase, leading to an increase in cAMP which cross activates PKG in the caveolae. No detectable increase in total cAMP level was detected as these changes occurred in the caveolae. These results are consistent with the notion that 17β-estradiol mediates its effect in the distinct microdomains of the caveolae of the plasma membrane with colocalization of adenylyl cyclase and PKG. © 2011 Elsevier Ltd.en_HK
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/issn/10436618en_HK
dc.relation.ispartofPharmacological Researchen_HK
dc.subjectcAMPen_HK
dc.subjectCaveolaeen_HK
dc.subjectEstrogenen_HK
dc.subjectNon-genomic effectsen_HK
dc.subjectPKGen_HK
dc.subjectVascular smooth muscleen_HK
dc.subject.meshAdenylate Cyclase - metabolism-
dc.subject.meshCyclic GMP-Dependent Protein Kinases - metabolism-
dc.subject.meshEstradiol - pharmacology-
dc.subject.meshMesenteric Artery, Superior - drug effects - enzymology-
dc.subject.meshVasodilator Agents - pharmacology-
dc.titleNon-genomic activation of adenylyl cyclase and protein kinase G by 17β-estradiol in vascular smooth muscle of the rat superior mesenteric arteryen_HK
dc.typeArticleen_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.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.phrs.2011.05.010en_HK
dc.identifier.pmid21641998-
dc.identifier.scopuseid_2-s2.0-80051799821en_HK
dc.identifier.hkuros201392en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80051799821&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume64en_HK
dc.identifier.issue5en_HK
dc.identifier.spage509en_HK
dc.identifier.epage516en_HK
dc.identifier.eissn1096-1186-
dc.identifier.isiWOS:000295913600011-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridKeung, W=19337708900en_HK
dc.identifier.scopusauthoridChan, MLY=54396830900en_HK
dc.identifier.scopusauthoridHo, EYW=54397134000en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridMan, RYK=7004986435en_HK
dc.identifier.citeulike9373850-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats