Gastrin-stimulated changes in Ca 2+ concentration in parietal cells depends on adenosine 3′,5′-cyclic monophosphate levels

Abstract

Background & Aims : The parietal cell has secretory receptors for histamine and acetylcholine, whereas the functional nature of the gastrin/cholecystokinin B receptor is controversial. This study in isolated gastric glands investigates the cholecystokinin B receptor—induced intracellular calcium concentration ([Ca] i) response in enterochromaffin-like (ECL) and parietal cells as a function of adenosine 3′,5′-cyclic monophosphate pathways. Methods : The responses of [Ca] i in ECL and parietal cells of perfused rabbit or rat calcium orange-loaded gastric glands were determined using confocal microscopy. ECL cells were identified by position, size, and autofluorescence and parietal cells by position and size. Results : Gastrin (1 μmol/L) produced an elevation of [Ca] i levels in both ECL and parietal cells. In the presence of 100 μmol/L cimetidine, the ECL cell response to gastrin was not affected but the [Ca] i response of the parietal cell was abolished. With dibutyryl adenosine 3′,5′ phosphate in addition to cimetidine, the response of the parietal cell [Ca] i to gastrin was restored in both the rat and rabbit. Conclusions : The [Ca] i response of the parietal but not the ECL cell to the addition of gastrin seems to depend on the presence of normal or elevated intracellular adenosine 3′,5′-cyclic monophosphate levels. Therefore, H 2 receptor activity may be permissive for the effect of gastrin on parietal cell function.