The present study shows that intravenous (i.v.) administration of morphine produces dose-dependent increases in tail flick and hot plate latencies in conscious rats. I.v. morphine also decreased heart rate, but had no significant effects on arterial blood pressure. Transection of the right vagus at the cervical level or pre-treatment with the peripherally acting opioid receptor antagonist naloxone methobromide attenuated the increased tail flick latency produced by either 1.75 or 2.5 mg/kg morphine. In addition, either right vagotomy or naloxone methobromide attenuated the increased hot plate latency produced by 1.75 mg/kg of morphine but not by 2.5 mg/kg of morphine. Following pre-treatment with naloxone methobromide, 1.75 and 2.5 mg/kg of morphine produced a small pressor response 1-3 min after injection. The bradycardia produced by 1.75 mg/kg of morphine was attenuated by naloxone methobromide, but not by right vagotomy. The bradycardia produced by 2.5 mg/kg of morphine was attenuated by either naloxone methobromide or vagotomy. These data obtained in the conscious rat are similar to previous reports using pentobarbital-anesthetized rats except for the following: (i) the dose-response function for inhibition of the tail flick was shifted to the right in conscious rats, (ii) the depressor response to morphine observed in anesthetized rats was attenuated in conscious rats, (iii) following naloxone methobromide, but not unilateral vagotomy, i.v. morphine produced a pressor response in the conscious rat, and (iv) unilateral vagotomy was not as effective in attenuating the antinociception and bradycardia in conscious rats as bilateral vagotomy is in pentobarbital-anesthetized rats. © 1993.