Role of gastrin/CCK-B receptor in the regulation of gastric acid secretion in rat.
Dig Dis Sci
; 42(9): 1901-7, 1997 Sep.
Article
en En
| MEDLINE
| ID: mdl-9331153
ABSTRACT
The aim of this study was to investigate whether gastrin regulates morphological changes and alpha-subunit gene expression in parietal cells through the gastrin/CCK-B receptor on enterochromaffin-like cells by histamine release. Treatment with 100 mg/kg of YM022, a potent and selective gastrin/CCK-B receptor antagonist, for one week in rats did not alter mRNA levels of histidine decarboxylase or H+, K+-ATPase. However, parietal cell morphology predominantly changed to the resting form, although the serum gastrin concentration was significantly increased. Additional treatment with YM022 and oral omeprazole, 100 mg/kg, for one week markedly suppressed the increases of mRNA levels of histidine decarboxylase and H+, K+-ATPase and completely blocked the morphological transformation of the parietal cells to a stimulated form induced by treatment with omeprazole alone. This indicates that the morphological transformation of parietal cells to an activated form with a subsequent increase in H+, K+-ATPase synthesis caused by hypergastrinemia is mediated by increased histidine decarboxylase gene expression in enterochromaffin-like cells via gastrin/CCK-B receptors.
Buscar en Google
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Células Parietales Gástricas
/
Gastrinas
/
Receptores de Colecistoquinina
/
Ácido Gástrico
Límite:
Animals
Idioma:
En
Revista:
Dig Dis Sci
Año:
1997
Tipo del documento:
Article
País de afiliación:
Japón