Abstract
Based on the current experimental evidence, a model is proposed for mutual interactions of histamine, prostaglandins, and cyclic AMP in regulation of gastric secretion and pathogenesis of peptic ulcer. Histamine acting on H2-receptor-associated adenylate cyclase stimulates cyclic AMP formation and consequently secretion of hydrochloric acid in oxyntic cells. Prostaglandins (mainly E type) in another cell population stimulate cyclic AMP formation which may lead to formation of glycosaminoglycans and glycoproteins. Glycosaminoglycans and glycoproteins may have antisecretory and cytoprotective properties. In addition to this effect, prostaglandin endoperoxides may inhibit histamine-stimulated cyclic AMP formation in oxyntic cells.
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