Peripheral beta-adrenergic blockade and activation of central alpha2-adrenergic receptors have parasympathomimetic effects. The impact of activation of central imidazoline I1-receptors on vagal activity is not yet clear, but there is some evidence that imidazoline I1-receptors agonists may inhibit the parasympathetic system. Parasympatholytic effects may represent a risk for patient with reduced parasympathetic activity. To clarify the effect of imidazoline I1-receptors stimulation on vagal activity, increasing doses of moxonidine were applied subcutaneously to rats with implanted telemetric transmitters. Heart rate and blood pressure variability and baroreflex sensitivity were analyzed. Both, low (0.04, 0.12, and 0.36 mg/kg) and high (1.08 and 3.24 mg/kg), doses of moxonidine reduced the low-frequency power of systolic pressure variability, an index of sympathetic vascular modulation. Despite this reduction, low moxonidine doses neither reduced heart rate nor increased baroreflex gain. A decline of very low frequency power of heart rate variability, a sign of parasympatholysis, was observed with low doses of moxonidine, which can explain the absence of change in heart rate. High doses of moxonidine profoundly augmented very low and high-frequency power of heart rate variability and baroreflex sensitivity. These data suggest that the stimulation of imidazoline I1-receptors is not only sympatholytic but also seems to have as well a weak parasympatholytic effect. However, high doses of moxonidine are strongly parasympathomimetic through the activation of central alpha2-adrenoceptors. Recruitment of alpha2-adrenoceptors also results in manifestation of several side effects.