Hemodynamic effect of 17β-estradiol in absence of NO in ovariectomized rats: Role of angiotensin II

Abstract

Previous reports correlate plasma levels of estrogen with increased nitric oxide (NO) production. To investigate whether the hemodynamic effects of estrogens are mediated by NO, we compared the hemodynamic changes induced by 17β-estradiol (100 μg/kg) in the absence and presence of the NO synthesis inhibitor N(ω)-nitro-L-arginine methyl ester (LNAME). All protocols were performed in ovariectomized, conscious rats. Estradiol alone resulted in no significant changes in cardiac index (CI) or mean arterial pressure (MAP). However, in the presence of L-NAME, estradiol induced a significant increase in total peripheral resistance (TPR) of 37.3 ± 11.7% and a decrease in CI of 27 ± 4.9%, without changes in MAP. Previous blockade of angiotensin II AT1 receptors with losartan prevented any change in CI and TPR induced by 17β-estradiol in the presence of L-NAME. These observations suggest that NO is necessary to offset a vasoconstrictor action of angiotensin II, which is stimulated by estradiol administration.