Skip Navigation


Cardiovascular Research Advance Access first published online on December 18, 2007
This version [Accepted Manuscript] published online on December 21, 2007
Cardiovascular Research, doi:10.1093/cvr/cvm112
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Supplementary Data
Right arrow All Versions of this Article:
78/1/130    most recent
cvm112v3
cvm112v2
cvm112v1
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Tang, E. H.
Right arrow Articles by Vanhoutte, P. M
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tang, E. H.
Right arrow Articles by Vanhoutte, P. M
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

The role of EP and TP receptors in the response to prostaglandin E2 in the aorta of WKY and spontaneously hypertensive rats

Eva HC Tang1, Boye Jensen2, Ole Skott2, George PH Leung1, Michel Feletou3, Ricky YK Man1 and Paul M Vanhoutte1,

1 Department of Pharmacology, The University of Hong Kong, Hong Kong
2 Department of Physiology and Pharmacology, University of Southern Denmark, Odense, Denmark
3 Department of Angiology, Institut de Recherches Servier, Suresnes, France

Corresponding Author: Paul M. Vanhoutte Department of Pharmacology, 2/F, Laboratory Block Faculty of Medicine Building, 21 Sassoon Road, Pokfulam The University of Hong Kong, Hong Kong Email: vanhoutte.hku{at}hku.hk; Tel: 852-28199250; Fax: 852-28170859

Aim: The present study examined the hypothesis that prostaglandin E2 (PGE2) through activation of prostaglandin E (EP) receptor contributes to endothelium-dependent contractions.

Methods and Results: Western blotting revealed that the protein expression of EP1 receptor was significantly down-regulated in the aorta of the spontaneously hypertensive rat (SHR), but there was no significant difference in the expression of EP2, EP4 and total EP3 receptors between preparations of Wistar Kyoto rats (WKY) and SHR. Isometric tension studies showed that low concentrations of PGE2 caused endothelium-dependent relaxations in WKY but not in aortas of the SHR. High concentrations of PGE2 evoked contractions predominately through the activation of thromboxane-prostanoid (TP) receptors in the WKY, but involves the dual activation EP and TP receptors in the SHR. SQ29,548, BAYu3405 and Terutroban (TP receptor antagonists), and AH6809 (non-selective EP receptor antagonist) abolished, while SC19220 (preferential EP1 receptor antagonist) did not inhibit endothelium-dependent contractions. Both SC19220 and AH6809 significantly inhibited contractions to U46619 [GenBank] (TP receptor agonist).

Conclusions: The present study demonstrates that the contraction caused by PGE2 in the SHR aorta is dependent on the activation of EP1 and TP receptors, but that endothelium-dependent contractions do not require the former. Thus, PGE2 is unlikely to be an endothelium-derived contracting factor in this artery. The ability of AH6809 to inhibit endothelium-dependent contractions can be attributed to its partial antagonism at TP receptors. Nevertheless, the impairment of PGE2-mediated relaxation may contribute to endothelial dysfunction in the aorta of the SHR.

Time for primary review: 24

This paper has been replaced with the correct article.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
A. Martorell, A. Sagredo, R. Aras-Lopez, G. Balfagon, and M. Ferrer
Ovariectomy increases the formation of prostanoids and modulates their role in acetylcholine-induced relaxation and nitric oxide release in the rat aorta
Cardiovasc Res, November 1, 2009; 84(2): 300 - 308.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
A. Virdis, R. Colucci, D. Versari, N. Ghisu, M. Fornai, L. Antonioli, E. Duranti, E. Daghini, C. Giannarelli, C. Blandizzi, et al.
Atorvastatin Prevents Endothelial Dysfunction in Mesenteric Arteries From Spontaneously Hypertensive Rats: Role of Cyclooxygenase 2-Derived Contracting Prostanoids
Hypertension, June 1, 2009; 53(6): 1008 - 1016.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
S. G. Denniss and J. W. E. Rush
Impaired hemodynamics and endothelial vasomotor function via endoperoxide-mediated vasoconstriction in the carotid artery of spontaneously hypertensive rats
Am J Physiol Heart Circ Physiol, April 1, 2009; 296(4): H1038 - H1047.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
K. Schror
Cyclooxygenase-2-Derived Prostaglandin F2{alpha}: An Endothelium-Derived Contractile Factor Acting Independently of Other Endothelium-Derived Contractile Factors via Vascular Thromboxane Receptors
Circ. Res., January 30, 2009; 104(2): 141 - 143.
[Full Text] [PDF]

Home page
 J. Physiol.Home page
P. M. Vanhoutte and E. H. C. Tang
Endothelium-dependent contractions: when a good guy turns bad!
J. Physiol., November 15, 2008; 586(22): 5295 - 5304.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.