Cholecystokinin satiety involves CCKA receptors perfused by the superior pancreaticoduodenal artery.

Abstract

Three experiments compared the potency of the type A cholecystokinin (CCKA)-receptor antagonist devazepide for increasing intake of 30% sucrose when injected into the superior pancreaticoduodenal (SPD) artery (SPD group) or jugular vein (IV group). In experiment 1, 15 min of sucrose intake in adult, male Sprague-Dawley rats after 6 h of food deprivation was increased by devazepide (20 micrograms/kg) administered into the SPD artery whether given alone or in conjunction with cholecystokinin octapeptide (CCK-8, 2 micrograms/kg ip). Devazepide had no effect in the IV group. In experiment 2, injection of 8, 20, and 50 micrograms/kg of devazepide into the SPD artery increased sucrose intake of nondeprived rats. Only the highest dose was effective in the IV group. On subsequent tests, administration of 1 microgram/kg of CCK-8 significantly suppressed intake only in the SPD group. In experiment 3, nondeprived rats with SPD artery and jugular vein catheters were tested in a within-subjects design. Devazepide (20 micrograms/kg) increased sucrose intake after injection into the SPD artery, but not into the jugular vein. In experiment 4, intraduodenal devazepide (8, 20, and 50 micrograms/kg) had no effect. These results indicate that CCKA receptors within the SPD arterial bed mediate the satiating action of CCK, consistent with local action of duodenal CCK.