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.