The effect of ranitidine on exocrine pancreatic secretion in the rat.
The effect of the H2-receptor antagonist ranitidine on pancreatic exocrine secretion was studied in the rat. In anaesthetized animals with acute fistulas pancreatic secretion was induced by central (2-deoxy-D-glucose, 2-DG) or peripheral (acetylcholine) cholinergic stimulants and by cholecystokinin and secretin. In some experiments cimetidine was used as a reference compound. Ranitidine (20 mg X kg-1 intraperitoneally) did not change neither basal secretion nor the response to the combined hormonal stimulation. On the contrary, it significantly increased 2-DG and acetylcholine-stimulated secretion, whereas cimetidine (100 mg X kg-1 intraperitoneally) inhibited the pancreatic response to 2-DG. The different behaviour of the two H2-antagonists suggests that the effect of ranitidine is independent of the H2-receptor blockade and most probably connected with the cholinergic-like action of the drug.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002766:Cholecystokinin / Q000494:pharmacology; D002927:Cimetidine / Q000494:pharmacology; D003847:Deoxyglucose / Q000494:pharmacology; D007274:Injections, Intraperitoneal; D008297:Male; D010179:Pancreas / Q000378:metabolism*; D011506:Proteins / Q000378:metabolism; D011899:Ranitidine / Q000008:administration & dosage / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000378:metabolism; D013268:Stimulation, Chemical
D011506:Proteins; D002927:Cimetidine; D011899:Ranitidine; D002766:Cholecystokinin; D003847:Deoxyglucose; D012964:Sodium; D000109:Acetylcholine