Clonidine, an alpha(2)-adrenoceptor agonist, was introduced to clinical practice in the 1960s because of its antihypertensive effect. It has several beneficial actions during the perioperative period, particularly for medically compromised patients. The objective of this study was to evaluate the effects of clonidine as a drug for intravenous conscious sedation. We assessed the effects of intravenous clonidine on the hemodynamic and sympathoadrenergic responses to nociceptive stimuli and we evaluated its sedative and analgesic effects. Twenty-five volunteers aged between 23 and 25 years were included in this study. They received clonidine intravenously at 2 microg/kg. Constant-current, square-wave stimuli were delivered as nociceptive stimuli to the median nerve of the arm. We measured blood pressure, heart rate, cardiac output, and plasma concentrations of noradrenaline, adrenaline, and cortisol. The sedative and analgesic effects were measured by visual analogue scales. Changes in heart rate and blood pressure were not significantly different between the clonidine and control groups. Cardiac output tended to decrease after clonidine administration. Clonidine exerted its greatest sedative effect 30 min after injection. Noradrenaline concentration reached its nadir 15 min after clonidine administration. The time course of adrenaline concentrations was similar to that of noradrenaline. The plasma concentration of cortisol decreased in both groups. The most common adverse effect was dry mouth. In conclusion, intravenous clonidine, at a dose of 2 microg/kg, did not induce significant bradycardia, hypotension, or severe side effects in the healthy volunteer. It attenuated the adrenergic response to electrical stimulation. The results suggested that clonidine is a useful drug for intravenous sedation.