ESTROGEN REPLACEMENT INCREASES BETA-ADRENOCEPTOR-MEDIATED RELAXATION OF RAT MESENTERIC-ARTERIES

The purpose of the present study was to determine whether estrogen rep lacement in ovariectomized rats could modulate arterial diameter respo nses to beta-adrenoceptor activation. Under relaxed conditions (0.1 mM papaverine) there were no differences in the lumen diameter of isolat ed, pressurized (50 mm Hg) mesenteric arteries from nontreated (191.7 +/- 13.8 mu m; n = 19) versus those from estrogen-treated (190.1 +/- 1 1 mu m; n = 14) ovariectomized Sprague-Dawley rats. In arteries precon tracted with noradrenaline (0.3-1 mu M), isoprenaline (0.01-10 mu M)-i nduced relaxation was significantly increased in arteries from ovariec tomized estrogen-treated rats (52.4 +/- 2% of the maximal relaxation i nduced by 0.1 mM papaverine, vs. 33.3 +/- 6.5%; p < 0.01). The half-ma ximal concentration value was 0.04 +/- 0.05 mu M in estrogen-treated r ats and 0.4 +/- 0.1 mu M in nontreated rats (p < 0.01). This response was inhibited by propranolol (1 mu M) in both groups to a comparable e xtent (61.5%), and was unaffected by endothelial removal. Forskolin (0 .01-10 mu M) induced similar concentration-dependent vasodilation in a rteries of both groups of rats with no differences in sensitivity or m aximal response. These results suggest that isoprenaline acts through beta-adrenoceptors present on vascular smooth muscle and that estrogen replacement enhances the relaxant responses induced by beta-adrenocep tor activation by an endothelium-independent mechanism.