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Article: Vascular effects of estrone and diethylstilbestrol in porcine coronary arteries

TitleVascular effects of estrone and diethylstilbestrol in porcine coronary arteries
Authors
KeywordsDiethylstilbestrol
Estrogens
Estrone
Vascular function
Issue Date2009
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.menopausejournal.com
Citation
Menopause, 2009, v. 16 n. 1, p. 104-109 How to Cite?
AbstractOBJECTIVE: To explore the effects of different estrogens on vascular function, we compared the vasorelaxant effects of 17β2-estradiol, 17β±-estradiol, estrone, and the synthetic estrogen diethylstilbestrol (DES) on porcine coronary arterial segments. DESIGN: Porcine coronary arterial rings were contracted with the stable thromboxane A2 analogue U46619 (3 × 10 M), and direct relaxation was examined by the addition of increasing concentrations of 17β2-estradiol, 17β±-estradiol, estrone, or DES (10 to 10 M). Modulation of agonist-induced contraction and relaxation was studied in coronary arterial rings incubated for 20 minutes with DES or estrone (10-10 M) with 17β2-estradiol (10 M) as comparison. RESULTS: Direct relaxation of arterial rings potentiated by these estrogens was recorded with a rank order potency of DES > 17β2-estradiol > estrone > 17β±-estradiol. 17β2-Estradiol potentiated relaxation responses to sodium nitroprusside and levcromakalim but not bradykinin or A23187 while reducing contractions to 5-hydroxytryptamine and U46619. DES and estrone, both at 10 M, mimicked the 17β2-estradiol-potentiated sodium nitroprusside and levcromakalim relaxation responses. Additionally, the inhibitory effects of 17β2-estradiol (10 M) on 5-hydroxytryptamine- and U46619-induced contractions were partially reproducible by DES (10 M) and estrone (10 M). CONCLUSIONS: Although DES is the most potent among the tested estrogenic compounds in eliciting relaxation, 17β2-estradiol is more effective than estrone and DES at enhancing endothelium-independent relaxation and reducing vascular contraction in porcine coronary arteries. Copyright © 2009 The North American Menopause Society.
Persistent Identifierhttp://hdl.handle.net/10722/59553
ISSN
2015 Impact Factor: 3.172
2015 SCImago Journal Rankings: 1.270
ISI Accession Number ID
Funding AgencyGrant Number
Committee on Research and Conference
University of Hong Kong
Funding Information:

Funding/Support: This study was Supported in part by a Committee on Research and Conference grant and a postdoctoral fellowship (H.T.) from the University of Hong Kong.

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.accessioned2010-05-31T03:52:35Z-
dc.date.available2010-05-31T03:52:35Z-
dc.date.issued2009en_HK
dc.identifier.citationMenopause, 2009, v. 16 n. 1, p. 104-109en_HK
dc.identifier.issn1072-3714en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59553-
dc.description.abstractOBJECTIVE: To explore the effects of different estrogens on vascular function, we compared the vasorelaxant effects of 17β2-estradiol, 17β±-estradiol, estrone, and the synthetic estrogen diethylstilbestrol (DES) on porcine coronary arterial segments. DESIGN: Porcine coronary arterial rings were contracted with the stable thromboxane A2 analogue U46619 (3 × 10 M), and direct relaxation was examined by the addition of increasing concentrations of 17β2-estradiol, 17β±-estradiol, estrone, or DES (10 to 10 M). Modulation of agonist-induced contraction and relaxation was studied in coronary arterial rings incubated for 20 minutes with DES or estrone (10-10 M) with 17β2-estradiol (10 M) as comparison. RESULTS: Direct relaxation of arterial rings potentiated by these estrogens was recorded with a rank order potency of DES > 17β2-estradiol > estrone > 17β±-estradiol. 17β2-Estradiol potentiated relaxation responses to sodium nitroprusside and levcromakalim but not bradykinin or A23187 while reducing contractions to 5-hydroxytryptamine and U46619. DES and estrone, both at 10 M, mimicked the 17β2-estradiol-potentiated sodium nitroprusside and levcromakalim relaxation responses. Additionally, the inhibitory effects of 17β2-estradiol (10 M) on 5-hydroxytryptamine- and U46619-induced contractions were partially reproducible by DES (10 M) and estrone (10 M). CONCLUSIONS: Although DES is the most potent among the tested estrogenic compounds in eliciting relaxation, 17β2-estradiol is more effective than estrone and DES at enhancing endothelium-independent relaxation and reducing vascular contraction in porcine coronary arteries. Copyright © 2009 The North American Menopause Society.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.menopausejournal.comen_HK
dc.relation.ispartofMenopauseen_HK
dc.rightsMenopause . Copyright © Lippincott Williams & Wilkins.en_HK
dc.subjectDiethylstilbestrolen_HK
dc.subjectEstrogensen_HK
dc.subjectEstroneen_HK
dc.subjectVascular functionen_HK
dc.titleVascular effects of estrone and diethylstilbestrol in porcine coronary arteriesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1072-3714&volume=16&spage=104&epage=109&date=2009&atitle=Vascular+effects+of+estrone+and+diethylstilbestrol+in+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.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/gme.0b013e3181813346en_HK
dc.identifier.pmid19131845-
dc.identifier.scopuseid_2-s2.0-64049114397en_HK
dc.identifier.hkuros156176en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-64049114397&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume16en_HK
dc.identifier.issue1en_HK
dc.identifier.spage104en_HK
dc.identifier.epage109en_HK
dc.identifier.eissn1530-0374-
dc.identifier.isiWOS:000262333100019-
dc.publisher.placeUnited Statesen_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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