The effect of secretagogue selection on potency determinations for gastric acid antisecretory agents.
The most common treatment for gastric and duodenal ulcers is by suppressing the secretion of gastric acid by the parietal cells of the stomach. Two major categories of drugs can accomplish this specifically: histamine H2-receptor antagonist and (H+ + K+)ATPase inhibitors. Using a canine model of gastric acid secretion and either histamine or food as secretagogues, the effects of two drugs from each of these classes were investigated. The two H2-antagonists (ranitidine, Wy-45,727) demonstrated a significantly greater antisecretory potency when acid secretion was stimulated by histamine as compared to a food stimulus. Conversely, the (H+ + K+)ATPase inhibitors (omeprazole, timoprazole) were equipotent regardless of stimulus.
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000251:Adenosine Triphosphatases / Q000037:antagonists & inhibitors*; D000818:Animals; D001562:Benzimidazoles / Q000494:pharmacology; D004285:Dogs; D005260:Female; D005502:Food; D005744:Gastric Acid / Q000378:metabolism*; D006632:Histamine / Q000494:pharmacology; D006635:Histamine H2 Antagonists / Q000494:pharmacology*; D009853:Omeprazole / Q000494:pharmacology; D011899:Ranitidine / Q000031:analogs & derivatives / Q000494:pharmacology
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D001562:Benzimidazoles; D006635:Histamine H2 Antagonists; C053415:WY 45727; D006632:Histamine; D011899:Ranitidine; C038402:timoprazole; D000251:Adenosine Triphosphatases; D009853:Omeprazole