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This Article Full Text Full Text (PDF) All Versions of this Article: 291/5/H2255    most recent 01115.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Gluais, P. Articles by Félétou, M. Search for Related Content PubMed PubMed Citation Articles by Gluais, P. Articles by Félétou, M.

In SHR aorta, calcium ionophore A-23187 releases prostacyclin and thromboxane A₂ as endothelium-derived contracting factors

¹Institut de Recherches Servier, Suresnes, France; and ²Department of Pharmacology, Faculty of Medicine, Hong Kong, China

Submitted 21 October 2005 ; accepted in final form 2 June 2006

In mature spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY), acetylcholine and the calcium ionophore A-23187 release endothelium-derived contracting factors (EDCFs), 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, whereas those released by A-23187 remain to be identified. Isometric tension and the release of PGs were measured in rings of isolated aortas of WKY and SHR. A-23187 evoked the endothelium-dependent release of prostacyclin, thromboxane A₂, PGF₂, PGE₂, and possibly PGH₂ (PGI₂ >> thromboxane A₂ = PGF₂ = 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 PGs 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 one-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 PGF₂, 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.

arteries; endothelial factors; hypertension; TP receptors; spontaneously hypertensive rats; Wistar-Kyoto rats

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