title: Effects of pantoprazole, a novel H+/K+-ATPase inhibitor, on duodenal ulcerogenic and healing responses in rats: a comparative study with omeprazole and lansoprazole.
abstract: BACKGROUND
  Pantoprazole, 2-[(2-pyridylmethyl) sulphinyl] benzimidazole, is a new substituted benzimidazole that inhibits the parietal cell H+/K+-ATPase.
  
  
  METHODS
  In the present study, the anti-secretory and anti-ulcer activities of pantoprazole were compared with those of omeprazole and lansoprazole in rats.
  
  
  RESULTS
  Pantoprazole (0.3-3 mg/kg, p.o.) as well as omeprazole (1-10 mg/kg, p.o.) and lansoprazole (1-10 mg/kg, p.o.) dose-dependently decreased both basal acid secretion in pylorus-ligated rats and the stimulated acid secretion induced by mepirizole in acute fistula rats, and the effects of pantoprazole were more potent than those of omeprazole and lansoprazole, the ED50 values for the stimulated acid secretion being 0.8, 2.0 and 1.2 mg/kg, respectively. Neither of these drugs had any effect on duodenal HCO3- secretion. These pump inhibitors prevented the development of duodenal lesions in response to mepirizole in a dose-related manner, the ED50 values for pantoprazole, omeprazole and lansoprazole being 0.4, 2.0 and 1.3 mg/kg, respectively. Likewise, pantoprazole showed the healing promoting action on chronic duodenal ulcers induced by acetic acid, and this effect was also more potent when compared to omeprazole or lansoprazole.
  
  
  CONCLUSIONS
  We conclude that pantoprazole exhibited both anti-ulcer and healing promoting effects on duodenal ulcers in rats, and the effects may be attributable to its potent anti-secretory action. Other pump inhibitors such as omeprazole and lansoprazole were almost equally effective as pantoprazole, yet this drug was most potent on the basis of ED50 values.
authors: Department of Pharmacology and Experimental Therapeutics, Kyoto Pharmaceutical University, Japan. takeuchi@mb.kyoto-phu.ac.jp
authors: K
authors: K
authors: Takeuchi
authors: A
authors: A
authors: Konaka
authors: M
authors: M
authors: Nishijima
authors: S
authors: S
authors: Kato
authors: T
authors: T
authors: Yasuhiro
mesh_terms: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D019342:Acetic Acid; D000818:Animals; D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D001562:Benzimidazoles / Q000627:therapeutic use*; D001639:Bicarbonates / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004381:Duodenal Ulcer / Q000139:chemically induced / Q000188:drug therapy*; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D004840:Epirizole; D005744:Gastric Acid / Q000378:metabolism; D064747:Lansoprazole; D008297:Male; D009853:Omeprazole / Q000031:analogs & derivatives* / Q000627:therapeutic use*; D000077402:Pantoprazole; D054328:Proton Pump Inhibitors; D051381:Rats; D017207:Rats, Sprague-Dawley; D013454:Sulfoxides / Q000627:therapeutic use*; D014945:Wound Healing / Q000187:drug effects
chemical_list: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000897:Anti-Ulcer Agents; D001562:Benzimidazoles; D001639:Bicarbonates; D004791:Enzyme Inhibitors; D054328:Proton Pump Inhibitors; D013454:Sulfoxides; D064747:Lansoprazole; D004840:Epirizole; D000077402:Pantoprazole; D009853:Omeprazole; D019342:Acetic Acid