Calcium, carbonic anhydrase and gastric acid secretion

Previous data concerning the action of calcium (Ca) on gastric acid secreti on (GAS) indicated that calcium ions increase GAS elicited by gastrin relea sed through a vagal mechanism, and also by a direct effect on parietal cell s. Our research showed that the stimulating effect of calcium on gastric ac id secretion can be antagonized by verapamil administration, which reduces gastric acid secretion. In the present study we followed the effect induced by administration of calcium and Ca-chelating agents (disodium EDTA) on ga stric acid secretion and on carbonic anhydrase (CA) activity. We selected t wo groups of healthy volunteers: Group I (n=21) received a single i.v. dose of CaCl2 (15 mg/kg b.w.), whereas Group II (n=22) received a single i.v. d ose of disodium EDTA (5 mg/kg b.w.). We determined blood calcium before and after treatment, gastric acid secretion at 2 hours, erythrocyte CA II acti vity, and CA IV activity in membrane parietal cells, which were isolated fr om gastric mucosa obtained by endoscopic biopsy. Assessment of carbonic anh ydrase activity was achieved by the stopped-flow method. In Group I calcium administration increased blood calcium, HCl output, CA II and CA IV activi ty as compared to initial values. In Group II, disodium EDTA reduced blood calcium, HCl output, CA II and CA IV activity as compared to initial values . The results demonstrated that increased blood calcium and GAS values afte r calcium administration correlated with the increase of erythrocyte CA II and parietal cell CA IV activity, while disodium EDTA induced a reversed pr ocess. Our results also show that cytosolic CA II and membrane CA IV values are sensitive to calcium changes and they directly depend on these levels. Our data suggest that intra- and extracellular pH changes induced by carbo nic anhydrase might account for the modulation of the physiological and pat hological secretory processes in the organism.