Alrestatin: gastric acid antisecretory-antiulcer activity in the rat.
Alrestatin sodium (AY-22,284-A) inhibited gastric acid secretion and decreased the volume of gastric juice produced in the pylorus-ligated rat when administered intraperitoneally or perorally. Pentagastrin-induced gastric acid output in the unanesthetized rat was antagonized. The pyloric ligation-induced ulcer formation in the rat was inhibited. Alrestatin sodium did not exhibit an anticholinergic profile. The drug did not block the norepinephrine neuronal uptake mechanism in rat brain or heart; it did not alter the endogenous norepinephrine concentration in the heart and decreased endogeneous brain norepinephrine concentration. Alrestatin sodium is an effective inhibitor of gastric acid secretion and ulcer formation in the rat.
D000449:Aldehyde Reductase / Q000037:antagonists & inhibitors*; D000818:Animals; D001921:Brain / Q000378:metabolism; D005260:Female; D005750:Gastric Juice / Q000378:metabolism*; D007546:Isoquinolines / Q000494:pharmacology* / Q000627:therapeutic use; D008297:Male; D009206:Myocardium / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D010276:Parasympatholytics / Q000494:pharmacology* / Q000627:therapeutic use; D010418:Pentagastrin / Q000494:pharmacology; D010627:Phenethylamines / Q000494:pharmacology; D011708:Pylorus / Q000502:physiology; D051381:Rats; D013276:Stomach Ulcer / Q000188:drug therapy; D013401:Sugar Alcohol Dehydrogenases / Q000037:antagonists & inhibitors*
D007546:Isoquinolines; D010276:Parasympatholytics; D010627:Phenethylamines; C016212:alrestatin; D013401:Sugar Alcohol Dehydrogenases; D000449:Aldehyde Reductase; D010418:Pentagastrin; D009638:Norepinephrine