Chronic ethanol attenuates centrally-mediated hypotension elicited via alpha-2-adrenergic, but not I1-imidazoline, receptor activation in female rats

摘要

Aims—This study dealt with the effect of chronic ethanol administration on hemodynamic responseselicited by α2-adrenergic (α-methyldopa) or I1-imidazoline (rilmenidine) receptor activation intelemetered female rats.Main methods—The effects of α-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 (BPand HR variability) in the absence or presence of ethanol, three time-domain indices of hemodynamicvariability were measured: (i) standard deviation of mean arterial pressure (SDMAP), (ii) standarddeviation of beat-to-beat intervals, and (iii) root mean square of successive differences in R-Rintervals.Key findings—In liquid diet-fed control rats, i.p. rilmenidine (600 μg/kg) or α-methyldopa (100mg/kg) reduced BP along with decreases and increases, respectively, in HR. Both drugs had no effecton HR variability but reduced BP variability (SDMAP), suggesting a reduced vasomotor sympathetictone. Ethanol feeding attenuated reductions in BP and SDMAP evoked by α-methyldopa but not byrilmenidine.Significance—We conclude that chronic ethanol preferentially compromises α2- but not I1-receptor-mediated hypotension in female rats probably via modulation of vasomotor sympatheticactivity. These findings highlight the adequacy of rilmenidine use to lower BP in hypertensivealcoholic females.