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Naloxone inhibition of pentagastrin‐stimulated gastric acid output in rats

An in situ stomach lumen‐perfusion technique is described for measuring the gastric acid output in anaesthetized rats. With this technique, 0.15 mol/l NaCl was continuously perfused into the gastric lumen and the outflowing perfusate was collected. The pH value of the out‐flowing perfusate was recorded every minute for 10 min, and after correcting for the change of volume, the pH values were converted into hydrogen ion activity. The basal gastric acid output in a group of 25 rats thus studied was 9.7 μmol H+/kg per 10 min (s.e.m. = 1.12, n= 25). Local blockade of opiate receptors in the gastric mucosa was performed by adding naloxone to the NaCl perfusate for 30 min. Naloxone at three concentrations, 0.1, 1, and 10 μmol/l, did not produce a significant change of the basal gastric output. Pentagastrin (0.05–20 μg/kg, i.v.) increased the basal gastric acid output in a dose‐dependent manner. Naloxone (10 μmol/l) significantly shifted the pentagastrin‐stimulated gastric acid output response curve to the right (P < 0.05, analysis of variance), and produced a sixfold change of pentagastrin dose. The results suggest that the opiate receptor in the gastric mucosa might affect gastric acid secretion by interacting with gastrin receptors. Local blockade of the opiate receptor by naloxone decreased the pentagastrin‐stimulated acid output.