I. Hernandez et al., HEMODYNAMIC-EFFECT OF 17-BETA-ESTRADIOL IN ABSENCE OF NO IN OVARIECTOMIZED RATS - ROLE OF ANGIOTENSIN-II, American journal of physiology. Regulatory, integrative and comparative physiology, 43(4), 1998, pp. 970-978
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.