Abstract
Stimuli originating in the small intestine enhance gastric acid secretion, an effect termed the intestinal phase of gastric secretion. A humoral agent, enterooxyntin (EO) may mediate this effect. Mechanical distension of an ex vivo-perfused segment of canine jejunum caused the release of EO measured by cytochemical quantification of hydroxyl ion production (HIP) in guinea pig gastric oxyntic cells, an index of acid secretion. The H2 receptor antagonist, cimetidine (10(-5) M), and diamine oxidase, which hydrolyzes endogenous histamine, reduced HIP by 60% and 48%, respectively. Atropine (10(-5) M), the muscarinic cholinergic antagonist, reduced HIP by 75%. EO-induced HIP was also inhibited partially by the Ca2+ antagonist EGTA (10(-6) M) and by blockade of calcium channels with LaCl3 (10(-6) M). EO does not appear to operate through any single pathway. EO may be a single substance, different from gastrin, or a mixture of substances that have stimulatory effects on the oxyntic cell. Its action on the oxyntic cell is apparently mediated by both histaminergic and cholinergic pathways. Since neither cimetidine nor atropine completely inhibited EO-induced HIP, a direct effect of EO on the oxyntic cell seems likely and appears to depend on Ca2+. Isolation and purification of EO will be necessary to better assess the potency, efficacy, and the detailed cellular mechanisms of EO action.
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