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Cardiovascular Research Advance Access originally published online on June 30, 2009
Cardiovascular Research 2009 84(2):300-308; doi:10.1093/cvr/cvp214
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Ovariectomy increases the formation of prostanoids and modulates their role in acetylcholine-induced relaxation and nitric oxide release in the rat aorta

Aina Martorell, Ana Sagredo, Rosa Aras-López, 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 ovarian function on thromboxane A2 (TXA2), prostaglandin (PG) I2, PGF2{alpha}, and PGE2 release as well as the role of these substances in nitric oxide (NO) release and acetylcholine (ACh)-mediated relaxation.

Methods and results: Aortic segments from ovariectomized and control female Sprague-Dawley rats were used. Cyclooxygenase (COX-1 and COX-2) expression was studied. ACh-induced relaxation was analysed 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 receptor antagonist SQ-29548. TXA2, PGI2, PGF2{alpha}, and PGE2 release was measured, and the vasomotor effect of exogenous TXA2, PGI2, PGF2{alpha}, and PGE2 was assessed. Basal and ACh-induced NO release in the absence and presence of NS-398, furegrelate, TCP, or TCP plus furegrelate was studied. Ovariectomy did not alter or increased COX-1 or COX-2 expression, respectively. NS-398 decreased, and furegrelate did not change, the ACh-induced relaxation in arteries from both groups. SQ29,548 decreased the ACh-induced relaxation only in aortas from ovariectomized rats. TCP decreased the ACh-induced relaxation in both groups, and furegrelate or SQ29,548 totally restored that response only in aortas from control rats. Ovariectomy increased the ACh-induced TXA2, PGI2, and PGE2 release and the contractile responses induced by exogenous TXA2, PGF2{alpha}, or PGE2, while it decreased the PGI2-induced vasodilator response. In aortas from control rats, NS-398 did not alter the ACh-induced NO release, and furegrelate, TCP, or TCP plus furegrelate increased that release. In arteries from ovariectomized rats, NS-398, furegrelate, TCP, or TCP plus furegrelate decreased the ACh-induced NO release.

Conclusion: Despite the prevalence of vasoconstrictor prostanoids derived from COX-2 in aortas from ovariectomized rats, the ACh-induced relaxation is maintained, probably as consequence of the positive regulation that prostanoids exert on eNOS activity.

KEYWORDS Ovarian function; TXA2; PGF2{alpha}; PGE2; PGI2; Endothelial NO; Rat aorta

Time for primary review: 20 days


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