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Am J Physiol Regul Integr Comp Physiol 284: R66-R75, 2003. First published October 3, 2002; doi:10.1152/ajpregu.00484.2002
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Vol. 284, Issue 1, R66-R75, January 2003

Effects of peripheral CCK receptor blockade on gastric emptying in rats

Roger D. Reidelberger1,2, Linda Kelsey1, Dean Heimann2, and Martin Hulce3

1 Veterans Affairs Medical Center, Omaha 68105, and 2 Departments of Biomedical Sciences and 3 Chemistry, Creighton University, School of Medicine, Omaha, Nebraska 68178

Type A CCK receptor (CCKAR) antagonists differing in blood-brain barrier permeability [devazepide penetrates; the dicyclohexylammonium salt of Nalpha -3-quinolinoyl-D-Glu-N,N-dipentylamide (A-70104) does not] were used to test the hypothesis that duodenal nutrient-induced inhibition of gastric emptying is mediated by CCKARs located peripheral to the blood-brain barrier. Rats received A-70104 (700 or 3,000 nmol · kg-1 · h-1 iv) or devazepide (2.5 µmol/kg iv) and either a 15-min intravenous infusion of CCK-8 (3 nmol · kg-1 · h-1) or duodenal infusion of casein, peptone, Intralipid, or maltose. Gastric emptying of saline was measured during the last 5 min of each infusion. A-70104 and devazepide abolished the gastric emptying response to a maximal inhibitory dose of CCK-8. Each of the macronutrients inhibited gastric emptying. A-70104 and devazepide attenuated inhibitory responses to each macronutrient. Intravenous injection of a CCK antibody to immunoneutralize circulating CCK had no effect on peptone or Intralipid-induced responses. Thus endogenous CCK appears to act in part by a paracrine or neurocrine mechanism at CCKARs peripheral to the blood-brain barrier to inhibit gastric emptying.

receptor antagonist; devazepide; A-70104; immunoneutralization; macronutrient


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