Endogenous estrogen mediates vascular reactivity and distensibility in pregnant rat mesenteric arteries

The role of estrogen in the maternal systemic cardiovascular adaptations du ring pregnancy is still controversial. Female Sprague-Dawley rats were impl anted at day 14 of pregnancy with either a 50-mg tamoxifen pellet (estrogen receptor blocker, n = 10) or placebo pellet (n = 10). Virgin female rats w ere a nonpregnant control (n = 7). At days 20-22 of pregnancy, resistance-s ized mesenteric arteries were mounted onto a dual-chamber arteriograph syst em. Pregnancy significantly blunted the pressor response to phenylephrine [ measurement of the effective concentration that yielded 50% maximum respons e (EC50) values were 1.5 +/- 0.22 vs. 0.69 +/- 0.16 muM (P < 0.05)] and enh anced vasodilation to ACh [EC50 = 1.13 +/- 2.53 vs. 3.13 +/- 6.04 nM (P < 0 .05)] compared with nonpregnant rats. However, tamoxifen treatment during p regnancy reversed these effects. Inhibition of nitric oxide (NO) synthase w ith N-G-monomethyl-L-arginine (250 muM) shifted only the responses of the p lacebo-treated pregnant group to both phenylephrine and ACh. Arterial diste nsibility in the placebo-treated pregnant group was also significantly incr eased (P < 0.05) compared with nonpregnant and tamoxifen-treated pregnant a nimals. In summary, endogenous estrogen during pregnancy increases NO-depen dent modulation of vessel tone and arterial distensibility.