CCK-8-stimulated insulin secretion in vivo is mediated by CCKA receptors.
The effects of the cholecystokinin A (CCKA) receptor antagonist, L-364,718, and the CCKB receptor antagonist, L-365,260, on CCK-8-stimulated insulin secretion were studied in vivo in the mouse. It was found that CCK-8-stimulated insulin secretion was suppressed by L-364,718 at a low dose level (0.078 mumol/kg). In contrast, L-365,260 caused a partial inhibition of CCK-8-stimulated insulin release only at the high dose level (24 mumol/kg). It is concluded that the CCK-8-stimulated insulin release in vivo is mediated by CCK receptors of the CCKA subtype.
Karlsson
S
S
Department of Pharmacology, Lund University, Sweden.
Ahrén
B
B
D000818:Animals; D001570:Benzodiazepinones / Q000494:pharmacology*; D020109:Devazepide; D007275:Injections, Intravenous; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D051379:Mice; D010671:Phenylurea Compounds; D011949:Receptors, Cholecystokinin / Q000037:antagonists & inhibitors / Q000378:metabolism*; D012844:Sincalide / Q000494:pharmacology*
D001570:Benzodiazepinones; D007328:Insulin; D010671:Phenylurea Compounds; D011949:Receptors, Cholecystokinin; C058121:L 365260; D020109:Devazepide; D012844:Sincalide