File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

Conference Paper: Modulation of vasoconstriction by testosterone in porcine coronary artery

TitleModulation of vasoconstriction by testosterone in porcine coronary artery
Authors
Issue Date2007
PublisherFederation of American Societies for Experimental Biology
Citation
Experimental Biology 2007, Washington, DC, 28 April–5 May 2007. In The FASEB Journal, 2007, v. 21 n. 6, p. A1160 How to Cite?
AbstractMen have a higher incidence of coronary heart disease than women at similar age until the age of 50. This finding has led to the hypothesis that testosterone may be a risk factor for coronary heart disease. However, the vascular actions of testosterone remain to be fully elucidated. The aim of this study was to investigate the relationship between testosterone and vascular reactivity, and the mechanism underlying this action. Changes in isometric tension were recorded in isolated rings of porcine coronary arteries. Rings, with disrupted endothelium, were incubated with testosterone in the absence or presence of various pharmacological inhibitors. Dose-response of the contraction agent, U46619 (a stable thromboxane A2 analogue), was then determined. Testosterone significantly enhanced contraction to U46619 in porcine coronary arteries. This effect of testosterone increased with increasing concentration, and was not affected by KT 5823 (a protein kinase G inhibitor). On the other hand, enhancement of U46619-induced contraction in porcine coronary arteries by testosterone was abolished by SQ 22536 (an adenylate cyclase inhibitor) or KT 5720 (a protein kinase A inhibitor). Our result suggested that the effect of testosterone on enhancement of contraction involved the cAMP pathway but not the cGMP pathway. This study was supported by a Committee on Research and Conference Grant from the University of Hong Kong.
Persistent Identifierhttp://hdl.handle.net/10722/106690
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorChan, PSen_HK
dc.contributor.authorLeung, SWSen_HK
dc.contributor.authorMan, RYKen_HK
dc.date.accessioned2010-09-25T23:26:23Z-
dc.date.available2010-09-25T23:26:23Z-
dc.date.issued2007en_HK
dc.identifier.citationExperimental Biology 2007, Washington, DC, 28 April–5 May 2007. In The FASEB Journal, 2007, v. 21 n. 6, p. A1160-
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/106690-
dc.description.abstractMen have a higher incidence of coronary heart disease than women at similar age until the age of 50. This finding has led to the hypothesis that testosterone may be a risk factor for coronary heart disease. However, the vascular actions of testosterone remain to be fully elucidated. The aim of this study was to investigate the relationship between testosterone and vascular reactivity, and the mechanism underlying this action. Changes in isometric tension were recorded in isolated rings of porcine coronary arteries. Rings, with disrupted endothelium, were incubated with testosterone in the absence or presence of various pharmacological inhibitors. Dose-response of the contraction agent, U46619 (a stable thromboxane A2 analogue), was then determined. Testosterone significantly enhanced contraction to U46619 in porcine coronary arteries. This effect of testosterone increased with increasing concentration, and was not affected by KT 5823 (a protein kinase G inhibitor). On the other hand, enhancement of U46619-induced contraction in porcine coronary arteries by testosterone was abolished by SQ 22536 (an adenylate cyclase inhibitor) or KT 5720 (a protein kinase A inhibitor). Our result suggested that the effect of testosterone on enhancement of contraction involved the cAMP pathway but not the cGMP pathway. This study was supported by a Committee on Research and Conference Grant from the University of Hong Kong.-
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology-
dc.relation.ispartofThe FASEB Journalen_HK
dc.titleModulation of vasoconstriction by testosterone in porcine coronary arteryen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLeung, SWS: swsleung@HKUCC.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.identifier.hkuros136365en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats