title: [Effects of gastric proton pump inhibitors on gastric secretion and peptic ulcers].
abstract: This is a review article on newly developed antisecretory drugs which are now called proton pump inhibitors. Gastric H+ is secreted from the secretory membrane of parietal cells into the lumen of the stomach, using energy obtained by destructing ATP with H+, K+-ATPase (proton pump). Various substituted benzimidazoles such as timoprazole, picoprazole, omeprazole, or NC-1300 potently inhibits this proton pump at pH 6.0, thereby resulting in a strong inhibition of gastric H+ secretion. This inhibition of H+ secretion lasts for a long period, ie, 1-3 days after a single oral or intraduodenal administration, both in experimental animals and humans. This long lasting activity of these compounds appears to be due to their accumulation in the parietal cells because of their low pKa values (about 4.0). Proton pump inhibitors dose-dependently inhibit the development of various experimental ulcers and accelerate healing of chronic gastric ulcers in animals. Since these compounds also potently inhibit the development of HCl X ethanol or HCl X aspirin-induced gastric ulcers in animals, they are considered to have a cytoprotective activity. Some of the compounds (e.g., omeprazole) afforded a complete healing of peptic ulcers in man when it was given once daily for 2 to 4 weeks, without any adverse effects. Therefore, these proton pump inhibitors appear to be promising drugs for the treatment of peptic ulcer diseases.
authors.forename: S
authors.initials: S
authors.lastname: Okabe
mesh_terms: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000251:Adenosine Triphosphatases / Q000037:antagonists & inhibitors*; D000818:Animals; D000897:Anti-Ulcer Agents / Q000009:adverse effects; D001241:Aspirin / Q000037:antagonists & inhibitors; D001562:Benzimidazoles / Q000008:administration & dosage / Q000494:pharmacology / Q000633:toxicity; D003994:Bucladesine / Q000037:antagonists & inhibitors; D004285:Dogs; D004381:Duodenal Ulcer / Q000188:drug therapy; D000431:Ethanol / Q000037:antagonists & inhibitors; D005750:Gastric Juice / Q000378:metabolism; D005753:Gastric Mucosa / Q000378:metabolism; D017506:H(+)-K(+)-Exchanging ATPase; D006635:Histamine H2 Antagonists / Q000494:pharmacology; D006801:Humans; D051379:Mice; D009853:Omeprazole; D010295:Parietal Cells, Gastric / Q000378:metabolism; D051381:Rats; D013276:Stomach Ulcer / Q000139:chemically induced / Q000188:drug therapy; D013329:Structure-Activity Relationship
chemical_list: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000897:Anti-Ulcer Agents; D001562:Benzimidazoles; D006635:Histamine H2 Antagonists; C048733:2-((2-dimethylaminobenzyl)sulfinyl)benzimidazole; D000431:Ethanol; D003994:Bucladesine; C038402:timoprazole; D000251:Adenosine Triphosphatases; D017506:H(+)-K(+)-Exchanging ATPase; D009853:Omeprazole; D001241:Aspirin; C028887:picoprazole