Amine trapping: physical explanation for the inhibitory effect of gastric acidity on the postprandial release of gastrin. Studies on rats and dogs.

We investigated the relationship between the pH dependence of meal-stimulated gastrin release and the permeability of the antral mucosa to dietary amines. This study was undertaken after previous work from our laboratory had demonstrated that dietary amines are potent in vivo and in vitro stimulants of gastrin release and that it is well established that amines are trapped in acidic environments. Three contrasting experimental model systems were employed to investigate the association of these two pH-dependent properties. In the first in vivo study, it was demonstrated that ingestion of standard rat Chow resulted in an increase in circulating gastrin and ammonia levels, whereas the postprandial increases in both properties were abolished if the rats ingested Chow that was preacidified to a pH of 2.4. Second, the antral uptake of the fluorescent cyclic amine, quinacrine, from the gastric lumen of pylorus-ligated rats was monitored by fluorescent microscopy and spectrophotometry and was demonstrated to be inhibited in a step-wise fashion as the luminal pH was decreased. Lastly, our in vitro studies suggested that the transport of [14C]methylamine into canine antral mucosa mounted in Ussing chambers was pH-dependent, as was gastrin release into the incubation medium. Thus, all the data are consistent with the possibility that meal-stimulated gastrin release is inhibited at low pH, due (in part) to the protonation of dietary amines, preventing their diffusion into the G cell to activate hormone secretion.