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Inhibition of gastric emptying and intestinal transit by amphetamine through a mechanism involving an increased secretion of CCK in male rats
Author(s) -
Doong MingLuen,
Lu ChienChen,
Kau MeiMei,
Tsai ShiowChwen,
Chiao YuChung,
Chen JiannJong,
Yeh JiunYih,
Lin Ho,
Huang SengWong,
Chen TsengShing,
Chang FullYoung,
Wang Paulus S.
Publication year - 1998
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0701937
Subject(s) - cholecystokinin , gastric emptying , amphetamine , medicine , proglumide , endocrinology , antagonist , cholecystokinin receptor , chemistry , receptor antagonist , pharmacology , receptor , stomach , dopamine
1 The effect of amphetamine on gastrointestinal (GI) transit and the plasma levels of cholecystokinin (CCK) were studied in male rats. 2 Gastric emptying was inhibited both acutely and chronically by the administration of amphetamine. GI transit was decreased by the acute administration of amphetamine but not affected by the chronic administration of amphetamine. 3 Plasma CCK levels were increased dose‐dependently by amphetamine. 4 Proglumide, a CCK receptor antagonist, prevented amphetamine‐induced inhibition of gastric emptying and the decrease in GI transit in male rats. 5 The selective CCK A receptor antagonist, lorglumide, dose‐dependently attenuated the amphetamine‐induced inhibition of gastric emptying in male rats. In contrast, the selective CCK B receptor antagonist, PD 135,158, did not reverse the effect of amphetamine on gastric emptying. 6 Both lorglumide and PD 135,158 reversed the inhibitory effect of amphetamine on GI transit in male rats. 7 These results suggest that amphetamine‐induced inhibition of gastric emptying and intestinal transit is due in part to a mechanism associated with the hypersecretion of endogenous CCK.British Journal of Pharmacology (1998) 124 , 1123–1130; doi: 10.1038/sj.bjp.0701937