Effect of naloxone and morphine on gastric acid secretion and on serum gastrin and pancreatic polypeptide concentrations in humans.
To evaluate the role of endogenous opiates on gastric acid secretion, we infused naloxone, a pure opiate antagonist drug, into 8 healthy subjects in the basal state and then after an amino acid meal. Naloxone significantly reduced basal acid secretion and the gastric acid secretory response to the meal. Maximum inhibition averaged 65% for basal acid secretion and 35% for meal-stimulated secretion. Naloxone had no effect on serum gastrin concentraitons or on the rate of gastric emptying of the meal. In the same subjects morphine also significantly reduced meal-stimulated acid secretion. In contrast to naloxone, morphine delayed gastric emptying and also enhanced the gastrin response to the meal. Morphine also abolished the pancreatic polypeptide response to the meal. Our studies with naloxone suggest that endogenous opiates may augment gastric acid secretion in humans. Failure of exogenous opitates to increase acid secretion suggests that actions other than opiate receptor stimulation (such as anticholinergic effects) may have come into play during morphine infusion.
D000293:Adolescent; D000328:Adult; D000596:Amino Acids / Q000008:administration & dosage; D005260:Female; D005746:Gastric Emptying / Q000187:drug effects; D005750:Gastric Juice / Q000378:metabolism*; D005755:Gastrins / Q000097:blood*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009020:Morphine / Q000494:pharmacology*; D009270:Naloxone / Q000494:pharmacology*; D010191:Pancreatic Polypeptide / Q000097:blood*
D000596:Amino Acids; D005755:Gastrins; D009270:Naloxone; D010191:Pancreatic Polypeptide; D009020:Morphine