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|Title:||Reduction of contractions to phenylephrine by L-NAME in the carotid artery of mice with endothelial overexpression of endothelin-1|
|Authors:||Baretella, OM;Li, FYL;Chung, SK;Vanhoutte, PM|
|Publisher:||Federation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/|
|Description:||Session - 1129. Endothelial Cell Biology - Poster: no. 1129.5|
The 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.
|Standard no:||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|
|Appears in Collections:||Department of Anatomy|
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