Effects of peripheral CCK receptor blockade on gastric emptying in rats.
Effects of peripheral CCK receptor blockade on gastric emptying in rats.
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外周 CCK 受体阻断对大鼠胃排空的影响。
DOI:
10.1152/ajpregu.00484.2002
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发表时间:
2003
期刊:
影响因子:
--
通讯作者:
Hulce,Martin
中科院分区:
文献类型:
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作者:
Reidelberger,RogerD;Kelsey,Linda;Heimann,Dean;Hulce,Martin
Type A CCK receptor (CCKAR) antagonists differing in blood-brain barrier permeability [devazepide penetrates; the dicyclohexylammonium salt ofNα-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−1iv) 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.