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| Content Provider | PubMed Central |
|---|---|
| Author | Céline, Rouaud Marcel, Delaforge Marielle, Anger-leroy Le, Filliatre Gaël Finet, Michel Hanf, Rémy |
| Copyright Year | 1999 |
| Abstract | Arachidonic acid (0.01–1μM) induced relaxation of precontracted rings of rabbit saphenous vein, which was counteracted by contraction at concentrations higher than 1μM. Concentrations higher than 1μM were required to induce dose-dependent contraction of vena cava and thoracic aorta from the same animals. Pretreatment with a TP receptor antagonist (GR32191B or SQ29548, 3μM) potentiated the relaxant effect in the saphenous vein, revealed a vasorelaxant component in the vena cava response and did not affect the response of the aorta. Removal of the endothelium from the venous rings, caused a 10 fold rightward shift in the concentration-relaxation curves to arachidonic acid. Whether or not the endothelium was present, the arachidonic acid-induced relaxations were prevented by indomethacin (10μM) pretreatment. In the saphenous vein, PGE2 was respectively a 50 and 100 fold more potent relaxant prostaglandin than PGI2 and PGD2. Pretreatment with the EP4 receptor antagonist, AH23848B, shifted the concentration-relaxation curves of this tissue to arachidonic acid in a dose-dependent manner. In the presence of 1μM arachidonic acid, venous rings produced 8–10 fold more PGE2 than did aorta whereas 6keto-PGF1α and TXB2 productions remained comparable. Intact rings of saphenous vein relaxed in response to A23187. Pretreatment with L-NAME (100μM) or indomethacin (10μM) reduced this response by 50% whereas concomitant pretreatment totally suppressed it. After endothelium removal, the remaining relaxing response to A23187 was prevented by indomethacin but not affected by L-NAME. We conclude that stimulation of the cyclo-oxygenase pathway by arachidonic acid induced endothelium-dependent, PGE2/EP4 mediated relaxation of the rabbit saphenous vein. This process might participate in the A23187-induced relaxation of the saphenous vein and account for a relaxing component in the response of the vena cava to arachidonic acid. It was not observed in thoracic aorta because of the lack of a vasodilatory receptor and/or the poorer ability of this tissue than veins to produce PGE2. |
| Related Links | http://dx.doi.org/10.1038/sj.bjp.0702265 |
| Ending Page | 44 |
| Page Count | 10 |
| Starting Page | 35 |
| File Format | |
| ISSN | 00071188 |
| Journal | British Journal of Pharmacology |
| Issue Number | 1 |
| Volume Number | 126 |
| Language | English |
| Publisher Date | 1999-01-01 |
| Access Restriction | Open |
| Subject Keyword | Pharmacology Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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