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Chanterelle Cadorette1 , Michèle Brochu1 , Jean St-Louis1
Laboratoire de pharmacologie vasculaire, Centre de recherche, Hôpital Sainte-Justine, Montréal, Québec, Canada 1
Pregnancy, in both human and rats, is accompanied by decreased arterial pressure, peripheral resistance and responses to vasoconstrictors. It was proposed that endothelium-dependent relaxation could be implicated in these manifestations of pregnancy through an increased production of nitric oxide or increased activity of its effector mechanisms. Among these, activation of potassium channels was suggested. We investigated the effects of blockade of KATP and KCa channels on carbachol-induced relaxation in aortic rings of term-pregnant and virgin rats. In phenylephrine (1µM) precontracted aortic rings, carbachol induced a concentration-dependent relaxation that was greater in rings of pregnant than virgin rats. In tissues of the latter, glibenclamide (1µM, KATP inhibitor) did not affect the relaxation-response curve to carbachol while TEA (0.5mM, KCa inhibitor) significantly reduced sensitivity and maximum relaxation to carbachol. In aorta of pregnant rats, although glibenclamide did not show any effect on responses to carbachol, it increased the reduction induced by TEA of carbachol relaxation. In both groups of aortic rings, inhibition of guanylate cyclase by methylene blue (10µM) totally prevented the carbachol-induced response. It is concluded that activation of K+ channels contributed to carbachol endothelium-dependent relaxation but the contribution of KATP and KCa channels appeared different in tissues of virgin and pregnant rats. Moreover, the activation of K+ channels in endothelium-dependent relaxation was shown to be the consequence of a cGMP-mediated mechanism. Furthermore, functional alterations of potassium channels were observed on pregnant rat endothelium-denuded aortic rings.
This abstract is being presented on Monday, August 2 at 8:00 AM to 10:15 AM at CUB 2nd Floor Ballroom.