Effects of 16, 16-dimethyl prostaglandin E2 on alkaline secretion in isolated canine gastric mucosa

Abstract

An isolated fundic mucosal preparation of dog stomach which is capable of exhibiting an alkaline secretion is described. A stable secretion was established 40 min to 1 hr after the mucosa was pretreated with the H2-antagonist cimetidine to block spontaneous acid output. Alkaline secretion decreased when Ca2+ was removed from the nutrient solution. This secretion was stimulated by dibutyryl cyclic GMP, but was not altered by acetylcholine, carbachol, or 16,16-dimethyl PGE2. Alkaline secretion from a similar antral mucosal preparation was stimulated by 16,16-dimethyl PGE2. We conclude that the 16,16-dimethyl PGE2-stimulated bicarbonate secretion previously demonstrated in in vivo canine fundic mucosa is not the result of a direct effect of PG on gastric mucosal cells and that an intact blood circulation or cholinergic innervation is required for this action to occur.

Stimulation of electrogenic chloride secretion by prostaglandin E2 in guinea‐pig isolated gastric mucosa.

“…Studies in vivo have shown that prostaglandins stimulate non-parietal secretion from mammalian stomach (rat: Bolton, Palmer & Cohen, 1978; dog: cat: Gascoigne & Hirst, 1981), and that this secretion consists principally of Na+ and Clions with smaller amounts of K+ and HC03-(dog: Miller, Henagan, Watkins & Loy, 1983;cat: Smeaton & Hirst, 1984;rat: Bunce, 1985). Studies on non-parietal secretion in mammalian isolated tissues have shown that 16,16-dimethyl-prostaglandin E2 stimulates bicarbonate secretion in rabbit gastric mucosa (Rees, Gibbons & Turnberg, 1983), although no such secretion was observed in dog gastric mucosa (Kuo, Miller & Shanbour, 1983). In contrast, in the latter tissue, Chaudhury & Jacobson (1978) found that 16,16-dimethyl-prostaglandin E2, rather than stimulating secretion, increased the rate of net sodium absorption across the mucosa.…”