The physiological mechanisms responsible for initiating gastrin release have assumed considerable interest because of their implication in peptic ulcer disease.
That a mechanical factor might play an important role in the stimulation of the gastric phase is deduced from the reports by Grossman et al,1 Dragstedt et al,2 and Grossman and Woodward.3
In 1964, Justin-Besançon et al4,5 studied the effect of metoclopramide hydrochloride on the autonomic nervous system, as well as its stimulating action on the gastrointestinal motor activity in man and experimental animals. These studies did not reveal a general parasympathomimetic activity attributable to the compound referred to.
Jacoby and Brodie6 showed that metoclopramide accelerated gastric emptying in rats and monkeys and that it stimulated stomach contractile activity in dogs. No significant increase in gastric acid secretion could be demonstrated in rats or dogs. The gastric motor stimulation brought about by matoclopramide was not