DUODENAL-ULCER - CALCIUM STATUS IN ISOLATED PARIETAL-CELLS

Although the etiology of duodenal ulcer is not known, its treatment wi th drugs that reduce acid secretion is well accepted. The central role of calcium in stimulus-secretion coupling resulting in acid secretion by gastric parietal cells is documented. However, the status of intra cellular calcium in gastric parietal cells in the basal state in patie nts with duodenal ulcer is not known. Multiple endoscopic gastric muco sal biopsies from the corpus of the stomach of 52 patients were proces sed and isolated parietal cells were studied. Intracellular calcium wa s estimated using fura-2-acetoxymethyl ester. Influx and efflux were d etermined by using radioactive calcium. Acridine orange retention was used to assess acid production. Only calcium influx at 20 min was sign ificantly (P < 0.01) more in patients with duodenal ulcer as compared to the control group. There was no difference between the groups in ca lcium influx at 0 and 60 min; calcium efflux at 0, 20, and 60 min; int racellular free calcium and acid secretion. We conclude that in the un stimulated state calcium homeostasis in isolated parietal cells of pat ients with duodenal ulcer shows only a minimal difference as compared to controls.