Calcium channel blocker decreases pentagastrin-stimulated alkaline-tide: A role for extracellular calcium in gastric acid secretion

We previously showed that repeated stimulation of the gastrin receptor may lead to down-regulation. We hypothesized that entry of extracellular Ca²⁺ may replenish cytosolic Ca²⁺ and enable continuation of the acid-secretion process. Pentagastrin-stimulated alkaline-tide study was performed in seven duodenal ulcer patients on 2 separate days - with and without pretreatment with verapamil (Ca²⁺ channel blocker). The alkaline-tide test may substitute the conventional gastric acid collection as previously described. A significant rise in base excess after pentagastrin injection was found on the first day of the study, from 0.400 ± 1.233 to 2.230 ± 1.330 (mean ± SD, P = 0.02). On the second day the rise was not statistically significant, from -0.200 ± 0.838 to 0.440 ± 1.200 (mean ± SD, P = 0.27). In 6 of the 7 patients the alkaline-tide decreased from 45.29 ± 21.75 mEq/45 min on the first day to 21.56 ± 17.48 mEq/45 min on the second day of the study (mean ± SD, P = 0.029), a decrease of 63.6 ± 36.2%. Our findings may support a dual source for Ca²⁺, the second messenger in gastrin-dependent gastric acid secretion. The first increase of intracellular Ca²⁺ comes from cellular stores, and the second from extracellular source by Ca²⁺ channels, which can be blocked by verapamil.