Our previous studies have demonstrated that acute ethanol administration counteracts imidazoline I 1 receptor but not α 2 -adrenoceptor-mediated hypotension in spontaneously hypertensive rats (SHR). In the present study, we investigated the effect of chronic ethanol administration on hypotensive responses elicited by acute administration of selective imidazoline I 1 receptor (rilmenidine) or α 2 -adrenoceptor (α-methyldopa) agonist along with ethanol effects on: (i) locomotor activity and (ii) time-domain indices of variability in blood pressure (standard deviation of mean arterial pressure) and heart rate (standard deviation of beat-to-beat intervals and root mean square of successive differences in R-R intervals). Hemodynamic and locomotor responses elicited by rilmenidine or α-methyldopa were assessed in radiotelemetered ethanol-fed (2.5% or 5% w/v, 12 week) and control SHR. In control SHR, i.p. rilmenidine (600 μg/kg) or α-methyldopa (100 mg/kg) significantly reduced blood pressure. Rilmenidine had no effect on heart rate whereas α-methyldopa elicited a biphasic response (tachycardia followed by bradycardia). Blood pressure and heart rate oscillations were also reduced by both drugs, which may conform to sympathoinhibition. The hypotensive effect of rilmenidine or α-methyldopa was significantly attenuated by ethanol feeding (2.5% or 5%) in a concentration-dependent manner. In addition, ethanol attenuated α-methyldopa-evoked reduction in heart rate, but not blood pressure, variability in marked contrast to attenuating rilmenidine-evoked reductions in blood pressure, but not heart rate, variability. These findings demonstrate that, unlike its acute effects, chronic ethanol attenuates both imidazoline I 1 receptor and α 2 -adrenoceptor-mediated hypotension whereas its effect on hemodynamic variability depended on the nature of the hypotensive stimulus.