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Cardiovascular Research Advance Access originally published online on November 5, 2007
Cardiovascular Research 2008 77(3):590-599; doi:10.1093/cvr/cvm059
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

Orchidectomy increases the formation of prostanoids and modulates their role in the acetylcholine-induced relaxation in the rat aorta

Aina Martorell, Javier Blanco-Rivero, Rosa Aras-López, Ana Sagredo, Gloria Balfagón and Mercedes Ferrer*

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

* Corresponding author. Tel: +34 91 497 3112; fax: +34 91 497 5478. E-mail address: mercedes.ferrer{at}uam.es

Aims: This study examines the effect of endogenous male sex hormones on thromboxane A2 (TXA2), prostaglandin (PG) I2, PGF2{alpha}, and PGE2 release, as well as their role in acetylcholine (ACh)-mediated relaxation in the aorta.

Methods and results: Aortic segments from orchidectomized and control male Sprague–Dawley rats were used to measure COX-2 protein expression. ACh-induced relaxation of these segments was also determined in the absence and presence of the COX-2 inhibitor NS-398, the TXA2 synthesis inhibitor furegrelate, the PGI2 synthesis inhibitor tranylcypromine (TCP), or the thromboxane-prostanoid (TP) receptor antagonist SQ-29 548. Furthermore, TXA2, PGI2, PGF2{alpha}, and PGE2 release as well as the vasomotor effect of exogenous TXA2, PGI2, PGF2{alpha}, and PGE2 were measured. COX-2 expression was increased in aortas from orchidectomized rats. NS-398 did not modify the ACh-induced relaxation in arteries from both control or orchidectomized rats. Furegrelate did not modify the ACh-induced relaxation in aortas from control animals but, in aortas from orchidectomized rats, it increased that response. TCP decreased the ACh-induced relaxation in both groups. The TP receptor antagonist, SQ29 548 failed to modify ACh-induced relaxation in aortas from either rat group. Pre-incubating arteries from orchidectomized rats with TCP plus furegrelate did not modify the decrease in the ACh response induced by TCP alone, but this response was restored by co-incubation of TCP plus SQ29 548. ACh-induced TXA2, PGI2, PGF2{alpha}, and PGE2 release were increased by orchidectomy. The presence of furegrelate plus TCP increased the ACh-induced PGE2 release more in arteries from orchidectomized than in those from control rats. The contractile responses induced by the TXA2 mimetic U-46619 or by exogenous PGF2{alpha} were similar in arteries from control and orchidectomized rats, while those induced by exogenous PGE2 were increased in arteries from orchidectomized rats; the vasodilator response induced by exogenous PGI2 was decreased in arteries from orchidectomized rats.

Conclusion: These data show that endogenous male sex hormone deprivation increases COX-2 expression, the release of TXA2, PGI2, PGF2{alpha}, and PGE2 and the contractile response induced by exogenous PGE2 and TXA2, while it decreases the relaxation induced by exogenous PGI2. Despite the predominance of vasoconstrictor prostanoids derived from COX-2 in aortas from orchidectomized rats, the ACh-induced relaxation remains increased.

KEYWORDS Male sex hormones; TXA2; PGF2{alpha}; PGE2; PGI2; Endothelium; Rat aorta

Time for primary review: 33 days


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