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Article: Enhanced relaxation of porcine coronary arteries after acute exposure to a physiological level of 17β-estradiol involves non-genomic mechanisms and the cyclic AMP cascade

TitleEnhanced relaxation of porcine coronary arteries after acute exposure to a physiological level of 17β-estradiol involves non-genomic mechanisms and the cyclic AMP cascade
Authors
Keywords17β-estradiol
Cyclic AMP
Cyclic AMP-dependent protein kinase
Cyclic GMP
Cyclic GMP-dependent protein kinase
Levcromakalim
Porcine coronary artery
Sodium nitroprusside
Issue Date2000
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, 2000, v. 129 n. 8, p. 1739-1747 How to Cite?
Abstract1. The present study extends our previous finding that the endothelium-independent relaxation in porcine coronary artery rings is enhanced after short-term (20 min) exposure to a physiological concentration (1 nM) of 17β-estradiol and demonstrates that this effect may be attributable to activation of the cyclic AMP pathway. 2. Isometric tension was recorded in isolated rings of porcine coronary arteries. 3. Relaxation by levcromakalim and sodium nitroprusside, but not bradykinin and calcium ionophore A23187, were significantly potentiated following 20 min treatment with 1 mM 17β-estradiol. This enhancing effect was insensitive to the transcriptional and translational inhibitors, actinomycin D and cycloheximide respectively and absent following repeated washing of the rings prior to construction of relaxation-response curves. 4. The potentiating actions of 1 nM 17β-estradiol on endothelium-independent relaxation were mimicked by the cyclic AMP analogue 8-Bromo-cyclic AMP and the protein kinase A activator Sp-cyclic AMPS but not by the cyclic GMP analogue 8-Bromo-cyclic GMP. The modulatory effect of 17β-estradiol was increased in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine. 5. The cyclic AMP-dependent protein kinase A inhibitor Rp-cyclic AMPS, but not the cyclic GMP antagonist Rp-8-Bromo-cyclic GMPS, effectively inhibited the enhancing effects 1 M 17β-estradiol had on the relaxation responses of levcromakalim and sodium nitroprusside. 6. These data support our earlier findings that physiologically relevant concentrations of 17β-estradiol can acutely modify vasorelaxation in vitro. Furthermore, we report that this short-term effect of 17β-estradiol on vasorelaxation appears to be mediated via non-genomic pathways and involves the cyclic AMP cascade.
Persistent Identifierhttp://hdl.handle.net/10722/49278
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTeoh, Hen_HK
dc.contributor.authorMan, RYKen_HK
dc.date.accessioned2008-06-12T06:38:20Z-
dc.date.available2008-06-12T06:38:20Z-
dc.date.issued2000en_HK
dc.identifier.citationBritish Journal Of Pharmacology, 2000, v. 129 n. 8, p. 1739-1747en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49278-
dc.description.abstract1. The present study extends our previous finding that the endothelium-independent relaxation in porcine coronary artery rings is enhanced after short-term (20 min) exposure to a physiological concentration (1 nM) of 17β-estradiol and demonstrates that this effect may be attributable to activation of the cyclic AMP pathway. 2. Isometric tension was recorded in isolated rings of porcine coronary arteries. 3. Relaxation by levcromakalim and sodium nitroprusside, but not bradykinin and calcium ionophore A23187, were significantly potentiated following 20 min treatment with 1 mM 17β-estradiol. This enhancing effect was insensitive to the transcriptional and translational inhibitors, actinomycin D and cycloheximide respectively and absent following repeated washing of the rings prior to construction of relaxation-response curves. 4. The potentiating actions of 1 nM 17β-estradiol on endothelium-independent relaxation were mimicked by the cyclic AMP analogue 8-Bromo-cyclic AMP and the protein kinase A activator Sp-cyclic AMPS but not by the cyclic GMP analogue 8-Bromo-cyclic GMP. The modulatory effect of 17β-estradiol was increased in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine. 5. The cyclic AMP-dependent protein kinase A inhibitor Rp-cyclic AMPS, but not the cyclic GMP antagonist Rp-8-Bromo-cyclic GMPS, effectively inhibited the enhancing effects 1 M 17β-estradiol had on the relaxation responses of levcromakalim and sodium nitroprusside. 6. These data support our earlier findings that physiologically relevant concentrations of 17β-estradiol can acutely modify vasorelaxation in vitro. Furthermore, we report that this short-term effect of 17β-estradiol on vasorelaxation appears to be mediated via non-genomic pathways and involves the cyclic AMP cascade.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.subjectCyclic AMPen_HK
dc.subjectCyclic AMP-dependent protein kinaseen_HK
dc.subjectCyclic GMPen_HK
dc.subjectCyclic GMP-dependent protein kinaseen_HK
dc.subjectLevcromakalimen_HK
dc.subjectPorcine coronary arteryen_HK
dc.subjectSodium nitroprussideen_HK
dc.titleEnhanced relaxation of porcine coronary arteries after acute exposure to a physiological level of 17β-estradiol involves non-genomic mechanisms and the cyclic AMP cascadeen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-1188&volume=129&issue=8&spage=1739&epage=1747&date=2002&atitle=Enhanced+relaxation+of+porcine+coronary+arteries+after+acute+exposure+to+a+physiological+level+of+17β-estradiol+involves+non-genomic+mechanisms+and+the+cyclic+AMP+cascadeen_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1038/sj.bjp.0703252en_HK
dc.identifier.pmid10780981-
dc.identifier.pmcidPMC1572009en_HK
dc.identifier.scopuseid_2-s2.0-0034003103en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034003103&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume129en_HK
dc.identifier.issue8en_HK
dc.identifier.spage1739en_HK
dc.identifier.epage1747en_HK
dc.identifier.isiWOS:000086809000027-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridTeoh, H=7003816542en_HK
dc.identifier.scopusauthoridMan, RYK=7004986435en_HK

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