| Abstract: | The aim of this study was to investigate whethergastrin regulates morphological changes andalpha-subunit gene expression in parietal cells throughthe gastrin/CCK-B receptor on enterochromaffin-likecells by histamine release. Treatment with 100 mg/kgof YM022, a potent and selective gastrin/CCK-B receptorantagonist, for one week in rats did not alter mRNAlevels of histidine decarboxylase or H+,K-ATPase. However, parietal cell morphology predominantlychanged to the resting form, although the serum gastrinconcentration was significantly increased. Additionaltreatment with YM022 and oral omeprazole, 100 mg/kg, for one week markedly suppressed theincreases of mRNA levels of histidine decarboxylase andH+, K-ATPase and completely blocked themorphological transformation of the parietal cells to astimulated form induced by treatment with omeprazolealone. This indicates that the morphologicaltransformation of parietal cells to an activated formwith a subsequent increase in H+, K-ATPasesynthesis caused by hypergastrinemia is mediated by increasedhistidine decarboxylase gene expression inenterochromaffin-like cells via gastrin/CCK-Breceptors. |
