HEMODYNAMIC-EFFECT OF 17-BETA-ESTRADIOL IN ABSENCE OF NO IN OVARIECTOMIZED RATS - ROLE OF ANGIOTENSIN-II

Previous reports correlate plasma levels of estrogen with increased ni tric oxide (NO) production. To investigate whether the hemodynamic eff ects of estrogens are mediated by NO, we compared the hemodynamic chan ges induced by 17 beta-estradiol (100 mu g/kg) in the absence and pres ence of the NO synthesis inhibitor N-omega-nitro-L-arginine methyl est er (L-NAME). All protocols were performed in ovariectomized, conscious rats. Estradiol alone resulted in no significant changes in cardiac i ndex (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 AT(1) re ceptors with losartan prevented any change in CI and TPR induced by 17 beta-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.