Prostaglandin-induced bicarbonate secretion in the canine stomach: characteristics and evidence for a cholinergic mechanism.

Using a canine chambered stomach preparation, the effect of topical 16,16-dimethyl prostaglandin E2 (dmPGE2) in neutral solution (150 mN NaCl) on gastric mucosal bicarbonate (HCO-3) secretion was assessed. Compared to control studies in which neutral solution alone bathed the epithelium, dmPGE2 (0.5, 1.0, 2.0, and 4.0 micrograms/ml), when applied to gastric mucosa, significantly increased the output of gastric HCO-3 in a stepwise and dose-related fashion. Accompanying these effects in HCO-3 output were similar increases in sodium, potassium, chloride, and gastric perfusate volume. IN other studies, the effects of intravenous atropine and close intraarterial tetrodotoxin on this PG-induced HCO-3 secretion were evaluated. Both agents completely prevented the stimulation of HCO-3 output induced by dmPGE2 (2 micrograms/ml). It is concluded that dmPGE2, when topically applied to canine gastric epithelium, is a potent stimulant of bicarbonate output that is dose-dependent. The ability of atropine and tetrodotoxin to prevent this secretion suggests that a cholinergic mechanism may be involved and that dmPGE2 mediates its effects on HCO-3 output through acetylcholine release which in turn stimulates cholinergic nerve endings.