Inhibition of gastric emptying by bombesin-like peptides is dependent upon cholecystokinin-A receptor activation

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

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

The amphibian peptide bombesin (BN) and the related mammalian peptides gastrin-releasing peptide (GRP) and neuromedin B (NMB) inhibit gastric emptying in rats. Exogenous administration of BN stimulates the release of cholecystokinin (CCK), a gastrointestinal peptide that also potently inhibits gastric emptying. To determine whether the inhibition of gastric emptying by BN-like peptides is mediated by a CCK-dependent mechanism, we examined the ability of the CCK-A receptor antagonist, devazepide, to block the inhibition of saline gastric emptying produced by BN, GRP18-27 and NMB. Using the same dosages as in the gastric emptying experiment, we also evaluated the effect of devazepide on feeding suppression produced by systemically administered BN. Our results showed that devazepide completely blocked the suppression of gastric emptying produced by BN, GRP18-27 and NMB but had no effect on BN-induced suppression of food intake. These results suggest that BN-like peptides inhibit gastric emptying through an indirect mechanism that is dependent upon CCK-A receptor activation. In contrast, the suppression of food intake by BN, in this experimental paradigm, is independent of CCK-A receptors. Copyright (C) 1999 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)101-106
Number of pages6
JournalRegulatory Peptides
Volume84
Issue number1-3
DOIs
StatePublished - Oct 22 1999
Externally publishedYes

Keywords

  • Devazepide
  • Gastrin-releasing peptide
  • Neuromedin B
  • Satiety

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Endocrinology
  • Clinical Biochemistry
  • Cellular and Molecular Neuroscience

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