Pharmacological dissociation of responses to CCK and gastric loads in rat mechanosensitive vagal afferents

G. J. Schwartz, P. R. McHugh, T. H. Moran

Research output: Contribution to journalArticle

66 Scopus citations

Abstract

To identify the transduction mechanisms underlying gastric vagal afferent responses to gastric loads and cholecystokinin (CCK), we investigated the ability of specific CCK antagonists, acute pylorectomy, and cholinergic blockade to effect these vagal afferent responses. The CCK-B antagonist L- 365,260 (10 pmol-1 nmol) failed to block the gastric vagal afferent response to gastric loads or 100 pmol CCK, while the CCK-A antagonist devazepide (100 pmol-100 nmol) competitively and dose dependently attenuated the response to CCK but not to gastric loads. Application of 100 nmol of the low-affinity CCK receptor antagonist CCK-JMV-180 also completely blocked the gastric vagal afferent response to 100 pmol CCK. Acute pylorectomy failed to block the gastric vagal afferent response to 100 pmol CCK or 2-ml gastric loads. Atropine sulfate administration (15 mg/rat) failed to block the gastric vagal afferent response to 100 pmol CCK or 2-ml gastric loads. These data suggest that 1) the vagal afferent response to CCK is mediated through CCK's interactions with vagal, rather than pyloric, CCK-A receptors, and 2) the vagal afferent responses to CCK and to gastric loads are mediated by dissociable, possibly independent, transduction mechanisms.

Original languageEnglish (US)
Pages (from-to)R303-R308
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume267
Issue number1 36-1
DOIs
StatePublished - 1994

Keywords

  • CCK- JMV-180
  • L-364,718
  • L-365,260
  • atropine
  • cholecystokinin type A receptor antagonist
  • cholecystokinin type B receptor antagonist
  • devazepide
  • gastric distension

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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