Comparison of the effect of omeprazole--a substituted benzimidazole--and ranitidine--a potent H2-receptor antagonist--on histamine-induced gastric acid secretion and the ultrastructure of canine parietal cells.

Gastric acid secretion and mucosal biopsy findings in canine stomach were evaluated after administration of omeprazole or ranitidine with and without histamine stimulation. Pretreatment with omeprazole (1 mg/kg) or ranitidine (0.5 mg/kg) almost completely prevented subsequent stimulation of acid secretion by histamine (40 micrograms/kg-h). Only ranitidine pretreatment, however, prevented post-histamine morphological transformation of parietal cells into the active state after histamine. Omeprazole pretreatment did not prevent the development of canaliculi and the reduction in the number of tubulovesicles in parietal cells after histamine. This canalicular expansion was, however, only partial with microvilli tightly packed together. Injection of omeprazole or ranitidine during half maximal stimulation by histamine effectively inhibited gastric acid secretion both in gastric fistulas (GF) and Heidenhain pouches (HP), and transformed the morphology of parietal cells into the resting state. In addition, omeprazole treatment with and without histamine stimulation increased the number of parietal cells with condensed mitochondria. This study demonstrates that omeprazole and ranitidine, while both potent inhibitors of gastric acid secretion, affect the parietal cell ultrastructure in different ways. Omeprazole does not prevent the formation of canaliculi in histamine-stimulated cells. This underscores the relative value of morphometrical studies of parietal cells.