Somatostatin is released in response to cholecystokinin by activation of type A CCK receptors

Kevin C K Lloyd, V. Maxwell, C. N. Chuang, H. C. Wong, A. H. Soll, J. H. Walsh

Research output: Contribution to journalArticle

30 Scopus citations

Abstract

Cholecystokinin is a principal mediator of intestinal fat-induced inhibition of gastric acid secretion, indicating that it is an important physiological enterogastrone. Cholecystokinin has been shown to inhibit acid secretion by activation of type A CCK receptors and through a mechanism involving somatostatin. In the present study, we investigated the possibility that these two mechanisms are directly related such that activation of type A CCK receptors by CCK causes the release of somatostatin. We tested this hypothesis in vivo in a study of CCK-stimulated release of somatostatin in dogs and in vitro in a study of CCK-stimulated release of somatostatin from an enriched culture of canine fundic D cells. In dogs, IV infusion of CCK (50 pmol/kg/h, IV) significantly increased circulating somatostatin concentrations above basal. Further, systemic administration of somatostatin MAb F(ab)1 fragments of a somatostatin monoclonal antibody prevented most of CCK-induced inhibition of meal-stimulated acid secretion. In canine fundic D cells in culture, CCK-stimulated somatostatin release was blocked in a dose-dependent fashion by application of a type A CCK receptor antagonist. This study indicates that CCK activates type A CCK receptors to release somatostatin from canine fundic mucosal D cells, and accounts for somatostatin-dependent CCK-induced inhibition of acid secretion.

Original languageEnglish (US)
Pages (from-to)223-227
Number of pages5
JournalPeptides
Volume15
Issue number2
DOIs
StatePublished - 1994

Keywords

  • Cholecystokinin (CCK)
  • D cells
  • Dog
  • Enterogastrone
  • Gastric acid secretion
  • Radioimmunoassay
  • Somatostatin

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Physiology
  • Cellular and Molecular Neuroscience

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