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1 Metabolisme, Institut de Recherches Servier, Suresnes, France
2 Angiologie, Institut de Recherches Servier, Suresnes, France
3 Surenes, France; Angiologie, Institut de Recherches Servier, Suresnes, France
4 Pharmacology, Faculty of Medicine, Hong Kong, China
* To whom correspondence should be addressed. E-mail: michel.feletou{at}fr.netgrs.com.
In mature spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY), acetylcholine and the calcium ionophore A 23187 release endothelium-derived contracting factors (EDCF), cyclooxygenase derivatives that activate thromboxane-endoperoxide (TP) receptors on vascular smooth muscle. The EDCFs released by acetylcholine are most likely prostacyclin and prostaglandin (PG) H2, while those released by A 23187 remain to be identified. Isometric tension and the release of prostaglandins were measured in rings of isolated aortas of WKY and SHR. A 23187 evoked the endothelium-dependent release of prostacyclin, thromboxane A2, PGF2a, PGE2 and possibly PGH2 (PGI2>>TXA2=PGF2a=PGE2). In SHR aortas, the release of prostacyclin and thromboxane A2 was significantly larger in response to A 23187 than to acetylcholine. In response to the calcium ionophore, the release of thromboxane A2 was significantly larger in aortas of SHR than in those of WKY. In both strains of rat, the inhibition of cyclooxygenase-1 prevented the release of prostaglandins and the occurrence of endothelium-dependent contractions. Dazoxiben, the thromboxane synthase inhibitor, abolished the A 23187-dependent production of thromboxane A2 and inhibited by approximately half the endothelium-dependent contractions. U 51605, an inhibitor of PGI-synthase, reduced the release of prostacyclin elicited by A 23187 but induced a parallel increase in the production of PGE2 and PGF2a, suggestive of a PGH2-spillover, which was associated with the enhancement of the endothelium-dependent contractions. These results indicate that in the aorta of SHR and WKY, the endothelium-dependent contractions elicited by A 23187 involve the release of thromboxane A2 and prostacyclin with a most likely concomitant contribution of PGH2.
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