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 language | English (US) |
|---|---|
| Pages (from-to) | 223-227 |
| Number of pages | 5 |
| Journal | Peptides |
| Volume | 15 |
| Issue number | 2 |
| DOIs | |
| State | Published - 1994 |
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Keywords
- Cholecystokinin (CCK)
- D cells
- Dog
- Enterogastrone
- Gastric acid secretion
- Radioimmunoassay
- Somatostatin
ASJC Scopus subject areas
- Biochemistry
- Endocrinology
- Physiology
- Cellular and Molecular Neuroscience
Cite this
Somatostatin is released in response to cholecystokinin by activation of type A CCK receptors. / Lloyd, Kevin C K; Maxwell, V.; Chuang, C. N.; Wong, H. C.; Soll, A. H.; Walsh, J. H.
In: Peptides, Vol. 15, No. 2, 1994, p. 223-227.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Somatostatin is released in response to cholecystokinin by activation of type A CCK receptors
AU - Lloyd, Kevin C K
AU - Maxwell, V.
AU - Chuang, C. N.
AU - Wong, H. C.
AU - Soll, A. H.
AU - Walsh, J. H.
PY - 1994
Y1 - 1994
N2 - 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.
AB - 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.
KW - Cholecystokinin (CCK)
KW - D cells
KW - Dog
KW - Enterogastrone
KW - Gastric acid secretion
KW - Radioimmunoassay
KW - Somatostatin
UR - http://www.scopus.com/inward/record.url?scp=0028178018&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028178018&partnerID=8YFLogxK
U2 - 10.1016/0196-9781(94)90006-X
DO - 10.1016/0196-9781(94)90006-X
M3 - Article
C2 - 7911992
AN - SCOPUS:0028178018
VL - 15
SP - 223
EP - 227
JO - Peptides
JF - Peptides
SN - 0196-9781
IS - 2
ER -