CCK-8 activates hepatic vagal C-fiber afferents

Academic Article


  • Intravenous administration of 2 μg/kg CCK-8 increased the single unit activity of 54% of hepatic vagal afferent fibers. Conduction velocity 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 μg/kg of the CCK(A) 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 hexamethonium 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 activation of CCK(A) receptors by CCK-8 increases hepatic vagal afferent activity and support the view that the duodenal satiety action of CCK is mediated by the hepatic branch.
  • Authors

    Published In

  • Brain Research  Journal
  • Digital Object Identifier (doi)

    Author List

  • Cox JE; Randich A
  • Start Page

  • 189
  • End Page

  • 194
  • Volume

  • 776
  • Issue

  • 1-2