Orchidectomy increases the formation of non-endothelial thromboxane A2 and modulates its role in the electrical field stimulation-induced response in rat mesenteric artery

The ann of this study was to analyze whether endogenous male sex hormones influence the release of thromboxane A, (TXA(2)) 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 TXA(2) release; EFS-induced response, nitric oxide (NO), norepinephrine (NA), and prostaglandin (PG) 1, 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 front 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 front orchidectomized rats. Furegrelate did not modify the EFS-induced NA release or vasoconstrictor response it) from either control or orchidectomized rats. The EFS-induced PGI(2) 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 TXA(2) release and ii) regulates the effect of endogenous TXA(2) on the EFS-induced response through different mechanisms that, at the least, involve the NO and PGI(2) systems. In arteries fiom control rats, inhibition of TXA, formation decreases the EFS-induced response by increasing neuronal NO release. In arteries from orchidectromized rats, the EFS-induced response is unaltered after the inhibition of TXA(2) formation, by increasing PGI(2) release.