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

Conference Paper: Reduction of contractions to phenylephrine by L-NAME in the carotid artery of mice with endothelial overexpression of endothelin-1

TitleReduction of contractions to phenylephrine by L-NAME in the carotid artery of mice with endothelial overexpression of endothelin-1
Authors
KeywordsBiology
Issue Date2012
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
The 2012 Annual Meeting of Experimental Biology (EB 2012), San Diego, CA., 21-25 April 2012. In The FASEB Journal, 2012, v. 26 meeting abstract, no. 1129.5 How to Cite?
AbstractThe release of endothelium-derived contracting factors (EDCF) is increased by exogenous endothelin-1 (ET-1). Experiments were designed to determine whether or not endothelial overexpression of ET-1 affects vascular responsiveness. Carotid artery rings with endothelium of control mice and mice with endothelial overexpression of ET-1 (TET-1) were contracted with the α1-adrenoceptor agonist phenylephrine in the absence or presence of the eNOS inhibitor L-NAME and exposed to acetylcholine. After washout, the rings were contracted with increasing concentrations of the TP receptor agonist U46619. EDCF-mediated increases in tension caused by acetylcholine were augmented in TET-1 arteries compared to controls both in the absence and presence of LNAME. In the presence of the latter, TET-1 rings showed stronger contractions to U46619 than controls. By contrast, contractions to phenylephrine were reduced by L-NAME in TET-1 arteries with a rightward shift and loss of the sigmoidal shape of the concentration-response curve. These results imply a role of endothelial ET-1 in EDCF-mediated contractions and indicate an increased TXA2 receptor signaling in vascular smooth muscle cells. They do not provide an explanation for the decreased response to α1-adrenergic activation in TET-1 arteries in the absence of NO.
DescriptionSession - 1129. Endothelial Cell Biology - Poster: no. 1129.5
Persistent Identifierhttp://hdl.handle.net/10722/165037
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorBaretella, OMen_US
dc.contributor.authorLi, FYLen_US
dc.contributor.authorChung, SKen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-09-20T08:13:46Z-
dc.date.available2012-09-20T08:13:46Z-
dc.date.issued2012en_US
dc.identifier.citationThe 2012 Annual Meeting of Experimental Biology (EB 2012), San Diego, CA., 21-25 April 2012. In The FASEB Journal, 2012, v. 26 meeting abstract, no. 1129.5en_US
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/165037-
dc.descriptionSession - 1129. Endothelial Cell Biology - Poster: no. 1129.5-
dc.description.abstractThe release of endothelium-derived contracting factors (EDCF) is increased by exogenous endothelin-1 (ET-1). Experiments were designed to determine whether or not endothelial overexpression of ET-1 affects vascular responsiveness. Carotid artery rings with endothelium of control mice and mice with endothelial overexpression of ET-1 (TET-1) were contracted with the α1-adrenoceptor agonist phenylephrine in the absence or presence of the eNOS inhibitor L-NAME and exposed to acetylcholine. After washout, the rings were contracted with increasing concentrations of the TP receptor agonist U46619. EDCF-mediated increases in tension caused by acetylcholine were augmented in TET-1 arteries compared to controls both in the absence and presence of LNAME. In the presence of the latter, TET-1 rings showed stronger contractions to U46619 than controls. By contrast, contractions to phenylephrine were reduced by L-NAME in TET-1 arteries with a rightward shift and loss of the sigmoidal shape of the concentration-response curve. These results imply a role of endothelial ET-1 in EDCF-mediated contractions and indicate an increased TXA2 receptor signaling in vascular smooth muscle cells. They do not provide an explanation for the decreased response to α1-adrenergic activation in TET-1 arteries in the absence of NO.-
dc.languageengen_US
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/-
dc.relation.ispartofThe FASEB Journalen_US
dc.subjectBiology-
dc.titleReduction of contractions to phenylephrine by L-NAME in the carotid artery of mice with endothelial overexpression of endothelin-1en_US
dc.typeConference_Paperen_US
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_US
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_US
dc.identifier.authorityChung, SK=rp00381en_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros210679en_US
dc.identifier.volume26-
dc.identifier.issuemeeting abstract-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats