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Article: Differential effects of 17β-estradiol and testosterone on the contractile responses of porcine coronary arteries

TitleDifferential effects of 17β-estradiol and testosterone on the contractile responses of porcine coronary arteries
Authors
Keywords17β-estradiol
Endothelium
Smooth muscle
Swine
Testosterone
Vasoconstriction
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. 7, p. 1301-1308 How to Cite?
Abstract1. We investigated the effects of short-term exposure to physiological levels of 17β-estradiol and testosterone on vasocontractile responses in porcine coronary artery rings. 2 .Concentration-response curves to endothelin-1, 5-hydroxytryptamine, the thromboxane analogue U46619 and KCl were constructed in endothelium-intact and endothelium-disrupted artery rings. 3. Thirty minutes exposure to 17β-estradiol (1 and 30 nM) significantly attenuated vasoconstriction to endothelin-1, 5-hydroxytryptamine and U46619. Conversely, the same concentrations of testosterone significantly potentiated responses elicited by these contractile agents. These inhibitory effects of 17β-estradiol and enhancing actions of testosterone on contractions were endothelium-independent. KCl-mediated contractions were unaffected by the presence of either sex hormones. 4. The oestrogen receptor antagonists, tamoxifen (10 μM) and ICI 182,780 (10 μM), were unable to reverse the inhibitory influence 1 nM 17β-estradiol had on the agonist-mediated contractile responses. Similarly, the androgen receptor antagonists, flutamide (10 μM) and cyproterone acetate (10 μM), failed to affect the potentiating activities of 1 nM testosterone. 5. The alteration in vasoconstrictive responses observed following acute exposure to either 1 nM 17β-estradiol and 1 nM testosterone were apparent even in the presence of the protein synthesis inhibitor cycloheximide (10 μM) and the transcription inhibitor actinomycin D (10 μM). 6. In conclusion, we report a unique type of sex hormone action on the coronary vasculature. These events occur at low nanomolar concentrations of 17β-estradiol and testosterone, are insensitive to conventional sex hormone receptor antagonists, are not blocked by de novo protein synthesis inhibitors and have rapid time-courses that are uncharacteristic of classical genomic activities.
Persistent Identifierhttp://hdl.handle.net/10722/49277
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.authorQuan, Aen_HK
dc.contributor.authorLeung, SWSen_HK
dc.contributor.authorMan, RYKen_HK
dc.date.accessioned2008-06-12T06:38:18Z-
dc.date.available2008-06-12T06:38:18Z-
dc.date.issued2000en_HK
dc.identifier.citationBritish Journal Of Pharmacology, 2000, v. 129 n. 7, p. 1301-1308en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49277-
dc.description.abstract1. We investigated the effects of short-term exposure to physiological levels of 17β-estradiol and testosterone on vasocontractile responses in porcine coronary artery rings. 2 .Concentration-response curves to endothelin-1, 5-hydroxytryptamine, the thromboxane analogue U46619 and KCl were constructed in endothelium-intact and endothelium-disrupted artery rings. 3. Thirty minutes exposure to 17β-estradiol (1 and 30 nM) significantly attenuated vasoconstriction to endothelin-1, 5-hydroxytryptamine and U46619. Conversely, the same concentrations of testosterone significantly potentiated responses elicited by these contractile agents. These inhibitory effects of 17β-estradiol and enhancing actions of testosterone on contractions were endothelium-independent. KCl-mediated contractions were unaffected by the presence of either sex hormones. 4. The oestrogen receptor antagonists, tamoxifen (10 μM) and ICI 182,780 (10 μM), were unable to reverse the inhibitory influence 1 nM 17β-estradiol had on the agonist-mediated contractile responses. Similarly, the androgen receptor antagonists, flutamide (10 μM) and cyproterone acetate (10 μM), failed to affect the potentiating activities of 1 nM testosterone. 5. The alteration in vasoconstrictive responses observed following acute exposure to either 1 nM 17β-estradiol and 1 nM testosterone were apparent even in the presence of the protein synthesis inhibitor cycloheximide (10 μM) and the transcription inhibitor actinomycin D (10 μM). 6. In conclusion, we report a unique type of sex hormone action on the coronary vasculature. These events occur at low nanomolar concentrations of 17β-estradiol and testosterone, are insensitive to conventional sex hormone receptor antagonists, are not blocked by de novo protein synthesis inhibitors and have rapid time-courses that are uncharacteristic of classical genomic activities.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.subjectEndotheliumen_HK
dc.subjectSmooth muscleen_HK
dc.subjectSwineen_HK
dc.subjectTestosteroneen_HK
dc.subjectVasoconstrictionen_HK
dc.titleDifferential effects of 17β-estradiol and testosterone on the contractile responses of porcine coronary arteriesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-1188&volume=129&issue=7&spage=1301&epage=1308&date=2000&atitle=Differential+effects+of+17β-estradiol+and+testosterone+on+the+contractile+responses+of+porcine+coronary+arteriesen_HK
dc.identifier.emailLeung, SWS: swsleung@hku.hken_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.authorityLeung, SWS=rp00235en_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1038/sj.bjp.0703164en_HK
dc.identifier.pmid10742284en_HK
dc.identifier.pmcidPMC1571960en_HK
dc.identifier.scopuseid_2-s2.0-0033624868en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033624868&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume129en_HK
dc.identifier.issue7en_HK
dc.identifier.spage1301en_HK
dc.identifier.epage1308en_HK
dc.identifier.isiWOS:000086138300005-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridTeoh, H=7003816542en_HK
dc.identifier.scopusauthoridQuan, A=7006871453en_HK
dc.identifier.scopusauthoridLeung, SWS=24540419500en_HK
dc.identifier.scopusauthoridMan, RYK=7004986435en_HK

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