Vagal cholinergic control of gastric alkaline secretion in normal subjects and duodenal ulcer patients

Gastric alkaline secretion was determined in ranitidine treated healthy subjects and duodenal ulcer (DU) patients using gastric perfusion aspiration system and back titration of gastric perfusate to original pH 6.0. Basal alkaline secretion showed periodic fluctuations reaching peaks at phase III of the migrating motor complex (MMC) in the stomach. Mean basal alkaline secretion in healthy normals and DU patients averaged 1120 ± 124 and 880 ± 72 μmol/h, respectively and no correlation was found between basal and maximally stimulated gastric acid and alkaline secretion. Modified sham feeding in normal subjects and in DU patients increased this secretion to the peaks of about 28 and 36% of the maximal alkaline response to intragastric application of 16,16 dimethyl-PGE in these subjects. Vagotomy did not affect significantly basal alkaline secretion but prevented the rise in alkaline secretion induced by modified sham feeding. Atropine (5-20 μg/kg) decreased dose dependently basal, and prevented the modified sham feeding induced alkaline secretion, while pirenzepine (5-20 μg/kg) had little infuence on basal, and did not affect the modified sham feeding induced, alkaline secretion. This study shows that basal gastric alkaline secretion fluctuates in phase with gastric motor activity, and is similar in normal and DU patients. Vagal stimulation strongly increases alkaline secretion, the effect being abolished by vagotomy and atropine, but not by pirenzepine, suggesting the involvement of M2 rather than M1 subtypes of muscarinic receptors in this stimulation.