Atropine inhibits meal-stimulated release of cholecystokinin.
To examine the effect of atropine on cholecystokinin (CCK) release, we studied CCK concentrations after a liquid fat meal in five volunteers both with and without pretreatment with atropine. In control studies peak plasma CCK 8 concentrations were 15.0 +/- 6.2 pmol l-1, and the integrated plasma CCK 8 response was 415 +/- 216 pmol l-1(2)h-1. Peak plasma CCK 33/39 concentrations were 16.5 +/- 4.6 pmol l-1, and integrated CCK 33/9 response was 469 +/- 200 pmol l-1(2)h-1. After pretreatment with atropine postprandial CCKs were undetectable (p less than 0.05 versus control studies). The abolition of measurable CCK release by atropine may entirely account for its inhibitory effects on biliary secretion and in part for its effect on the pancreas.
D000328:Adult; D001285:Atropine / Q000494:pharmacology*; D002766:Cholecystokinin / Q000097:blood / Q000378:metabolism* / Q000031:analogs & derivatives; D005227:Fatty Acids / Q000008:administration & dosage; D005260:Female; D005502:Food; D006801:Humans; D008297:Male; D010446:Peptide Fragments / Q000097:blood; D012844:Sincalide / Q000097:blood
D005227:Fatty Acids; D010446:Peptide Fragments; C032740:cholecystokinin 39; D001285:Atropine; D002766:Cholecystokinin; D012844:Sincalide