Omeprazole

Hydrochloric acid (HCl) secretion into the gastric lumen is a process regulated mainly by the H(+)/K(+)-ATPase of the proton pump, expressed in high quantities by the parietal cells of the stomach. ATPase is an enzyme on the parietal cell membrane that facilitates hydrogen and potassium exchange through the cell, which normally results in the extrusion of potassium and formation of HCl (gastric acid).

Omeprazole is a member of a class of antisecretory compounds, the substituted benzimidazoles, that stop gastric acid secretion by selective inhibition of the H+/K+ ATPase enzyme system. Proton-pump inhibitors such as omeprazole bind covalently to cysteine residues via disulfide bridges on the alpha subunit of the H+/K+ ATPase pump, inhibiting gastric acid secretion for up to 36 hours. This antisecretory effect is dose-related and leads to the inhibition of both basal and stimulated acid secretion, regardless of the stimulus.

Mechanism of H. pylori eradication

Peptic ulcer disease (PUD) is frequently associated with Helicobacter pylori bacterial infection (NSAIDs). The treatment of H. pylori infection may include the addition of omeprazole or other proton pump inhibitors as part of the treatment regimen. H. pylori replicates most effectively at a neutral pH. Acid inhibition in H. pylori eradication therapy, including proton-pump inhibitors such as omeprazole, raises gastric pH, discouraging the growth of H.pylori. It is generally believed that proton pump inhibitors inhibit the urease enzyme, which increases the pathogenesis of H. pylori in gastric-acid related conditions.