Chronic ethanol attenuates centrally-mediated hypotension elicited via alpha(2)-adrenergic, but not I(1)-imidazoline, receptor activation in female rats.

AIMS This study dealt with the effect of chronic ethanol administration on hemodynamic responses elicited by alpha(2)-adrenergic (alpha-methyldopa) or I(1)-imidazoline (rilmenidine) receptor activation in telemetered female rats. MAIN METHODS The effects of alpha-methyldopa or rilmenidine on blood pressure (BP), heart rate (HR) and their variability were investigated in rats that received liquid diet without or with ethanol (5% w/v) for 12 weeks. To evaluate the effect of each drug on cardiovascular autonomic control (BP and HR variability) in the absence or presence of ethanol, three time-domain indices of hemodynamic variability were measured: (i) standard deviation of mean arterial pressure (SDMAP), (ii) standard deviation of beat-to-beat intervals, and (iii) root mean square of successive differences in R-R intervals. KEY FINDINGS In liquid diet-fed control rats, i.p. rilmenidine (600 microg/kg) or alpha-methyldopa (100 mg/kg) reduced BP along with decreases and increases, respectively, in HR. Both drugs had no effect on HR variability but reduced BP variability (SDMAP), suggesting a reduced vasomotor sympathetic tone. Ethanol feeding attenuated reductions in BP and SDMAP evoked by alpha-methyldopa but not by rilmenidine. SIGNIFICANCE We conclude that chronic ethanol preferentially compromises alpha(2)- but not I(1)-receptor-mediated hypotension in female rats probably via modulation of vasomotor sympathetic activity. These findings highlight the adequacy of rilmenidine use to lower BP in hypertensive alcoholic females.