Abstract
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 language | English (US) |
---|---|
Pages (from-to) | R1726-R1733 |
Journal | American Journal of Physiology - Regulatory Integrative and Comparative Physiology |
Volume | 272 |
Issue number | 6 41-6 |
DOIs | |
State | Published - 1997 |
Externally published | Yes |
Keywords
- C fibers
- Gastric tension receptors
- Ingestive behavior
- Satiety
- Vagal cholecystokinin binding
- Visceral afferents
ASJC Scopus subject areas
- General Medicine