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Substituted benzimidazoles inhibit gastric acid secretion stimulated by histamine, pentagastrin and vagal innervation. In contrast to anticholinergic agents and H2-receptor antagonists these compounds also block secretion induced by exogenous cyclic AMP suggesting a more peripheral site of action. Recent data show that these substances inhibit a H+/K+-ATPase which is localized at the secretory surface of the parietal cells and is generally regarded as the proton pump within the gastric mucosa. Because of the unique distribution of H+/K+-ATPase the inhibitory action of substituted benzimidazoles may offer a new therapeutic approach in hypersecretory states.
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