STIMULATION OF ALKALINE SECRETION IN AMPHIBIAN-ISOLATED GASTRIC-MUCOSA BY 16,16-DIMETHYL PGE2 AND PGF2-ALPHA - PROPOSED EXPLANATION FOR SOME OF THE CYTOPROTECTIVE ACTIONS OF PROSTAGLANDINS

  • 1 January 1979
    • journal article
    • research article
    • Vol. 76  (3) , 497-503
Abstract
The mechanism of the gastric cytoprotective action of prostaglandins is unknown but seems to be unrelated to inhibition of acid secretion. Effect of the prostaglandins, 16,16-dimethyl E2 and F2.alpha. on H+ and .**GRAPHIC**. secretion and electrical properties in amphibian-isolated gastric mucosa were studied. Spontaneous net secretion fundic mucosa from Rana temporaria and Necturus was acid; Necturus antrum secreted only .**GRAPHIC**. 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 HCO3-secretion in R. temporaria fundus. The drug (10-5 M) also stimulated antral alkalinization. There was a dose-related increase in .**GRAPHIC**. 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. Gastric .**GRAPHIC**. secretion may have 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.