Our previous studies showed that the hypotensive effect of chronic
ethanol in female rats is reduced by
ovariectomy (OVX) rats and was restored after
estrogen replacement (OVXE(2)). Further, in randomly cycling rats, chronic
ethanol increased cardiac parasympathetic dominance and subsequently reduced myocardial contractility and blood pressure (BP). In this study, we tested the hypothesis that alterations in myocardial contractility and sympathovagal control account for the E(2) exacerbation of the hemodynamic effects of
ethanol. BP, myocardial contractility (+dP/dt(max)), and spectral cardiovascular autonomic profiles were evaluated in radiotelemetered OVX, and OVXE(2) rats receiving liquid diet with or without
ethanol (5%, w/v) for 13 weeks. In OVX rats,
ethanol caused modest
hypotension along with significant increases in +dP/dt(max) during weeks 2-5. The high-frequency (IBI(HF), 0.75-3 Hz) and low-frequency (IBI(LF), 0.25-0.75 Hz) bands of interbeat intervals were briefly increased and decreased, respectively, by
ethanol. Compared with its effects in OVX rats, chronic treatment of OVXE(2) rats with
ethanol elicited significantly greater and more sustained reductions in systolic (SBP) and diastolic (DBP) blood pressures and +dP/dt(max). Altered sympathovagal balance and parasympathetic overactivity were more evident in
ethanol-treated OVXE(2) rats as suggested by the sustained: (i) increases in high-frequency bands of interbeat intervals (IBI(HF), 0.75-3 Hz), and (ii) decreases in low-frequency IBI bands (IBI(LF), 0.25-0.75 Hz), IBI(LF/HF) ratio and +dP/dt(max). The plasma
ethanol concentration was not affected by changes in the hormonal milieu. These findings suggest that
estrogen exacerbates the
ethanol-evoked reductions in myocardial contractility and BP and the associated parasympathetic overactivity in female rats.