Effect of cholecystokinin variant (CCK39) on dispersed acinar cells from guinea pig pancreas.
In dispersed acinar cells from guinea pig pancreas, cholecystokinin variants (CCK39 and CCK33) or carboxyl-terminal octapeptide of cholecystokinin (CCK-OP) caused significant increases in outflux of 45Ca, cyclic GMP, and release of amylase. In homogenates of acinar cells each peptide caused a significant increase in adenylate cyclase activity. For each function tested (1) CCK39 was equipotent with with CCK33, (2) CCK39 and CCK33 were 10 to 30 times less potent than CCK-OP, (3) the efficacies of CCK39, CCK33, and CCK-OP were the same, and (4) none of these effects were altered by concentrations of atropine sufficient to abolish the action of muscarinic cholinergic agents.
D000262:Adenylyl Cyclases / Q000378:metabolism; D000681:Amylases / Q000378:metabolism; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002766:Cholecystokinin / Q000031:analogs & derivatives* / Q000494:pharmacology; D006152:Cyclic GMP / Q000378:metabolism; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008297:Male; D010179:Pancreas / Q000187:drug effects*
D001285:Atropine; D002766:Cholecystokinin; D000681:Amylases; D000262:Adenylyl Cyclases; D006152:Cyclic GMP; D002118:Calcium