Pupillary and cardiac responses to i.v. injection of detomidine (1-30 micrograms/kg), a novel veterinary sedative analgesic, were observed in rats anesthetized with pentobarbital. Detomidine caused a dose-dependent mydriasis and bradycardia. The alpha 2-adrenoceptor antagonist, yohimbine (0.1-1.0 mg/kg, i.v.), prevented the detomidine-induced mydriasis in a dose-dependent manner. The nonselective alpha-adrenoceptor antagonist, tolazoline at 6 mg/kg, i.v., also prevented the detomidine-induced mydriasis. However, tolazoline at 3 mg/kg, i.v., was not effective in preventing this effect of detomidine. The alpha 1-adrenoceptor antagonist, prazosin at 1.5 mg/kg, i.v., did not reduce the detomidine-induced mydriasis. In contrast to what was found with mydriasis, none of the antagonists at the doses studied prevented detomidine-induced bradycardia. When yohimbine was given i.v., 5 min after the last dose of detomidine (30 micrograms/kg), it promptly and completely reversed mydriasis in all groups. However, yohimbine reversed detomidine-induced bradycardia only in the control group and in the animals pretreated with 1.5 mg prazosin/kg or 3 mg tolazoline/kg. The results suggested that the mydriatic effect of detomidine was mediated by the alpha 2-adrenoceptors, and that mydriasis was a good model for studying alpha 2-adrenoceptor agonists and antagonists. Although the results suggested that the bradycardia effect of detomidine was partially mediated by alpha 2-adrenoceptors, other unknown mechanisms might also be involved.