In humans, plasma beta-endorphin levels rise during application of acute stressful stimuli (vertigo, cold pain, and transcutaneous electrical stimulation) that induce gut motor disturbances. Whereas it is possible that circulating beta-endorphin participates in the mediation of these central effects on gut motility, its role cannot be established solely on the basis of changes in plasma levels. Therefore, we designed the present study to investigate 1) the dose-related effects of intravenous synthetic human beta-endorphin and naloxone on gastrointestinal pressure activity in fed healthy individuals; and 2) the interactions of the opiate agonist and antagonist. Infusion of beta-endorphin increased pyloric phasic pressure activity (P less than 0.001) and induced intestinal bursts of rhythmic activity (P less than 0.05) which interrupted normal fed motility. These effects were dose related, with the pyloric dose-response profile being essentially linear. The effects in the proximal intestine were obtained with doses of beta-endorphin at 250 ng X kg-1 X min-1 or greater. In the antrum, there was an overall reduction in phasic pressure activity (P less than 0.02), which was predominantly an effect of the highest dose of beta-endorphin infused (2,500 ng X kg-1 X min-1). Naloxone by itself had no significant effect on fed upper gut motility. However, naloxone significantly inhibited the effect of the lower doses of beta-endorphin on the pylorus. In addition, naloxone significantly reduced the probability of beta-endorphin, triggering intestinal bursts of rhythmic activity. These data suggest that beta-endorphin may play a humoral role in the stimulation of fed pyloric contraction at physiological levels.(ABSTRACT TRUNCATED AT 250 WORDS)