CCK-8 ACTIVATES HEPATIC VAGAL C-FIBER AFFERENTS

Intravenous administration of 2 mu g/kg CCK-8 increased the single uni t activity of 54% of hepatic vagal afferent fibers. Conduction velocit y tests indicated that all of these units were C fibers. The increase in hepatic vagal activity produced by CCK-8 was significantly reduced by i.v. administration of 200 mu g/kg of the CCKA receptor antagonist devazepide. Control comparisons indicated that this reduction was not an artifact of tachyphylaxis resulting from repeated administration of CCK-8. Further, the inability of pretreatment with atropine and hexam ethonium to reduce the increases in hepatic vagal activity produced by CCK-8 suggests that the latter effect was not secondary to changes in gastrointestinal motor function. These outcomes demonstrate that acti vation of CCKA receptors by CCK-8 increases hepatic vagal afferent act ivity and support the view that the duodenal satiety action of CCK is mediated by the hepatic branch. (C) 1997 Elsevier Science B.V.