Stimulation of alkaline secretion in amphibian-isolated gastric mucosa by 16,16-dimethyl PGE2 and PGF2 alpha. A proposed explanation for some of the cytoprotective actions of prostaglandins.

The mechanism of the gastric cytoprotective action of prostaglandins is unknown but seems to be unrelated to inhibition of acid secretion. In the present study, effects of the prostaglandins, 16,16-dimethyl E2 and F2 alpha on H+ and HCO-3 secretion and electrical properties in amphibian-isolated gastric mucosa were studied. Spontaneous net secretion in fundic mucosa from Rana temporaria and Necturus was acid, whereas Necturus antrum secreted only HCO-3. The histamine H2-receptor antagonist, metiamide (10(-3) M), was used to inhibit acid secretion for studies on fundic alkalinization. Nutrient side administration of 16,16-dimethyl E2 (10(-6) M) for 60 min inhibited H+ secretion and stimulated HCO-3 secretion in Rana temporaria fundus. The drug (10(-5) M) also stimulated antral alkalinization. There was a dose-related increase in HCO-3 secretion in Necturus fundus after administration of F2 alpha (10(-5)-10(-4) M), but this drug had no significant effect on H+ secretion. Inhibition of acid secretion by 16,16-dimethyl E2 was associated with an increase in potential difference (PD), but there was no change in electrical resistance. Neither of the prostaglandins affected PD or resistance in alkaline-secreting tissues. Previous work has suggested that gastric HCO-3 secretion has a physiologic role in protecting the mucosal surface. The ability of prostaglandins to stimulate alkaline secretion may contribute to the cytoprotective action of these drugs in the stomach.