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Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid, C/Arzobispo Morcillo 4, 28029 Madrid, Spain

(Correspondence should be addressed to M Ferrer; Email: mercedes.ferrer{at}uam.es)

The aim of this study was to analyze whether endogenous male sex hormones influence the release of thromboxane A₂ (TXA₂) and its role in the electrical field stimulation (EFS)-induced response, as well as the mechanism involved. For this purpose, endothelium-denuded mesenteric arteries from control and orchidectomized male Sprague–Dawley rats were used to measure TXA₂ release; EFS-induced response, nitric oxide (NO), norepinephrine (NA), and prostaglandin (PG) I₂ release were also measured in the presence of the TXA₂ synthesis inhibitor furegrelate. Orchidectomy increased basal and EFS-induced TXA₂ release. Furegrelate decreased the EFS-induced contraction in arteries from control rats, but did not modify it in arteries from orchidectomized rats. The EFS-induced neuronal NO release and vasodilator response were increased by furegrelate in arteries from control rats, but were not modified in arteries from orchidectomized rats. Furegrelate did not modify the EFS-induced NA release or vasoconstrictor response in arteries from either control or orchidectomized rats. The EFS-induced PGI₂ release was not modified by furegrelate in arteries from control rats, but was increased in arteries from orchidectomized rats. The results of the present study show that endogenous male sex hormone deprivation i) increases non-endothelial TXA₂ release and ii) regulates the effect of endogenous TXA₂ on the EFS-induced response through different mechanisms that, at the least, involve the NO and PGI₂ systems. In arteries from control rats, inhibition of TXA₂ formation decreases the EFS-induced response by increasing neuronal NO release. In arteries from orchidectomized rats, the EFS-induced response is unaltered after the inhibition of TXA₂ formation, by increasing PGI₂ release.

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