The present studies investigated the role of beta adrenergic receptors in mediating arousal from anesthesia and the effects of stress on this process. In support of previous findings by others, it was found that blockade of beta-1 and beta-2 receptors by propranolol delayed arousal from halothane anesthesia and that this effect was attributable to blockade of beta-1 receptors because it was duplicated by betaxolol but not by ICI 118,551. Restraint stress also produced a delay in arousal from both halothane and hexobarbital anesthesia. This effect, which was observed at 0.5 but not 24 h after the stress, could not be explained by a stress-induced alteration in the metabolism of the anesthetic, as no difference in brain concentration of hexobarbital was found between stressed and control mice. The parallel effects of beta-1 blockade and stress further supports the hypothesis that stress produces an impairment in function at either the beta-1 receptor or some process coupled to this receptor.