The adrenocortical, hyperglycemic, and hemodynamic responses to cholecystectomy or vagotomy were studied in 16 patients under halothane and N2O/O2 anesthesia. The patients were randomly divided into two groups: eight patients received naloxone in doses used clinically (2.5 microgram/kg i.v.) just before induction of anesthesia, while eight subjects received placebo. The results showed insignificant differences in plasma concentrations of cortisol and glucose between groups. Nor did blood pressure, heart rates, and inspired halothane concentrations differ significantly between groups. Thus, inhibition of opiate receptors and endorphins by naloxone in an otherwise clinically effective dosage does not influence the adrenocortical, hyperglycemic, or hemodynamic responses to surgical stress. We therefore conclude from our data that opiate receptors and endorphins are not involved in the initial phase of the endocrine-metabolic responses to surgery nor are they part of the neural mechanisms mediating stress-induced analgesia.