[Inhibition of acid secretion with substituted benzimidazole. A new principle in ulcer therapy?].
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.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D001562:Benzimidazoles / Q000627:therapeutic use*; D000242:Cyclic AMP / Q000494:pharmacology; D004791:Enzyme Inhibitors; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000187:drug effects*; D006632:Histamine / Q000494:pharmacology; D006801:Humans; D010418:Pentagastrin / Q000494:pharmacology; D013276:Stomach Ulcer / Q000188:drug therapy*
D001562:Benzimidazoles; D004791:Enzyme Inhibitors; D006632:Histamine; D000242:Cyclic AMP; D000251:Adenosine Triphosphatases; D010418:Pentagastrin
Säuresekretionshemmung durch substituierte Benzimidazole. Ein neues Prinzip in der Ulkustherapie?