Interaction of calcium and gastrin on gastric acid secretion in duodenal ulcer patients

SUMMARY A dose response study of the effect on gastric acid secretion of synthetic human gastrin-17 in doses of 50, 200, and 500 ng/kg/h was performed in eight healthy volunteers and in eight patients with duodenal ulcer. The study was repeated on a separate day during intravenous infusion of calcium gluconate (0.1 mmol Ca +/kg/h). In healthy subjects the acid response to the combined infusion of synthetic human gastrin and calcium did not significantly exceed the response to synthetic human gastrin alone, in contrast with patients with duodenal ulcer in whom the combined infusion did significantly improve acid output compared with infusion of synthetic human gastrin alone. The dose of synthetic human gastrin required for half maximal acid response (D50) was reduced in both groups but significantly more in patients with duodenal ulcer. No difference in serum gastrin concentrations or in serum calcium concentrations were found. It is hypothesised that extracellular calcium plays a role in gastrin stimulated acid secretion in man and that patients with duodenal ulcer are more sensitive to this calcium dependent mechanism than non-duodenal ulcer subjects. Calcium may participate in the stimulation of gastric acid secretion in man by a dual mechanism- that is, by gastrin release ' 2 and by an action directly on the parietal cell.1 3 In previous studies it was found that calcium increases the sensitivity of the parietal cells to synthetic human gastrin in healthy subjects.3 Furthermore, that administration of verapamil decreases the sensitivity of the parietal cells to gastrin, suggesting that influx of calcium into the parietal cells is an essential step in the acid secretory process. The aim of the present study has been to investigate whether calcium dependence of the parietal cells is quantitatively different in normal subjects and patients with duodenal ulcer