In humans, plasma β-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 β-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 β-endorphin and naloxone on gastrointestinal pressure activity in fed healthy individuals; and 2) the interactions of the opiate agonist and antagonist. Infusion of β-endorphin increased pyloric phasic pressure activity (P < 0.001) and induced intestinal bursts of rhythmic activity (P < 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 β-endorphin at 250 ng.kg-1.min-1 or greater. In the antrum, there was an overall reduction in phasic pressure activity (P < 0.02), which was predominantly an effect of the highest dose of β-endorphin infused (2,500 ng.kg-1.min-1). Naloxone by it self had no significant effect on fed upper gut motility. However, naloxone significantly inhibited the effect of the lower doses of β-endorphin on the pylorus. In addition, naloxone significantly reduced the probability of β-endorphin, triggering intestinal bursts of rhythmic activity. These data suggest that β-endorphin may play a humoral role in the stimulation of fed pyloric contraction at physiological levels. Furthermore, β-endorphin exhibits strong pharmacoligical actions on fed antral and intestinal motility in humans.
|Original language||English (US)|
|Journal||American Journal of Physiology - Gastrointestinal and Liver Physiology|
|State||Published - 1986|
ASJC Scopus subject areas
- Physiology (medical)