Helicobacter pylori augments the acid inhibitory effect of omeprazole on parietal cells and gastric H+/K+-ATPase

Background-In duodenal ulcer patients, intragastric acidity during omeprazo le treatment is significantly lower before Helicobacter pylori eradication than after cure. Aims-To determine if H pylori enhances the acid inhibitory potency of omepr azole in isolated parietal cells and on H+/K+-ATPase. Methods-Rat. parietal cells and pig gastric membrane vesicles enriched in H +/K+-ATPase activity were incubated with H pylori and the H pylori fatty ac id cis 9,10-methyleneoctadecanoic acid (MOA), and the inhibitory effects of omeprazole on parietal cell acid production, H+/K+-ATPase enzyme activity, and ATPase mediated proton transport were assessed. Results-In isolated parietal cells, H pylori and MOA increased the acid inh ibitory potency of omeprazole 1.8 fold. H pylori did not affect the inhibit ory potency of omeprazole on H+/K+-ATPase enzyme activity. in proton transp ort studies, H pylori (intact bacteria and sonicate) and MOA accelerated th e onset of the inhibitory effect of omeprazole and enhanced the proton diss ipation rate in response to omeprazole. H pylori itself increased proton pe rmeability at the vesicle membrane. Conclusion-Our results show that H pylori augments the acid inhibitory pote ncy of omeprazole in parietal cells and enhances omeprazole induced proton efflux rate from gastric membrane vesicles. We suggest that omeprazole unma sks the permanent effect of H pylori on proton permeability at the apical p arietal cell membrane, which is counteracted in the absence of a proton pum p inhibitor by a reserve H+/K+-ATPase capacity.