Relationships between gastric motility and gastric vagal afferent responses to CCK and GRP in rats differ

Gary J. Schwartz, Timothy H. Moran, Wesley O. White, Ellen E. Ladenheim

Research output: Contribution to journalArticlepeer-review

48 Scopus citations


The brain-gut peptides cholecystokinin (CCK) and the mammalian bombesin-like peptide gastrin-releasing peptide (GRP) suppress food intake. Vagotomy blocks CCK- but not bombesin (BN)-induced feeding suppression, demonstrating differential vagal contributions. We examined the relationship between the ability of CCK and the active fragment of GRP, GRP-(1827), to stimulate gastric vagal afferent activity and their ability to elicit changes in gastric motility. We also examined ligated cervical vagal segments and revealed specific 125I-CCK vagal binding without evidence of radiolabeled BN binding sites. Both close arterial and intraperitoneal CCK and GRP-(1827) produced dose-dependent increases in activity in gastric vagal mechanoreceptive afferents. CCK dose dependently decreased gastric pressure without altering antral wall tension, whereas GRP-(1827) dose dependently increased both gastric pressure and peak antral wall muscle tension. These results suggest that GRP-(1827) activates gastric vagal afferents secondary to its stimulation of gastric motor effects. CCK activates this same population of vagal afferents independent of changes in gastric tension, suggesting a direct action of CCK at functional vagal CCK receptors.

Original languageEnglish (US)
Pages (from-to)R1726-R1733
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Issue number6 41-6
StatePublished - 1997
Externally publishedYes


  • C fibers
  • Gastric tension receptors
  • Ingestive behavior
  • Satiety
  • Vagal cholecystokinin binding
  • Visceral afferents

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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