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Am J Physiol Heart Circ Physiol 280: H956-H961, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 3, H956-H961, March 2001

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

Yunlong Zhang, Ken G. Stewart, and Sandra T. Davidge

Perinatal Research Centre, Department of Obstetrics and Gynecology, and Department of Physiology, University of Alberta, Edmonton, Alberta T6G 2S2, Canada

The role of estrogen in the maternal systemic cardiovascular adaptations during pregnancy is still controversial. Female Sprague-Dawley rats were implanted 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 were a nonpregnant control (n = 7). At days 20-22 of pregnancy, resistance-sized mesenteric arteries were mounted onto a dual-chamber arteriograph system. Pregnancy significantly blunted the pressor response to phenylephrine [measurement of the effective concentration that yielded 50% maximum response (EC50) values were 1.5 ± 0.22 vs. 0.69 ± 0.16 µM (P < 0.05)] and enhanced 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 pregnancy reversed these effects. Inhibition of nitric oxide (NO) synthase with NG-monomethyl-L-arginine (250 µM) shifted only the responses of the placebo-treated pregnant group to both phenylephrine and ACh. Arterial distensibility in the placebo-treated pregnant group was also significantly increased (P < 0.05) compared with nonpregnant and tamoxifen-treated pregnant animals. In summary, endogenous estrogen during pregnancy increases NO-dependent modulation of vessel tone and arterial distensibility.

nitric oxide; pregnancy; endothelium


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