Effect of cholecystokinin-2 receptor blockade on rat stomach ECL cells - Ahistochemical, electron-microscopic and chemical study

Citation
D. Chen et al., Effect of cholecystokinin-2 receptor blockade on rat stomach ECL cells - Ahistochemical, electron-microscopic and chemical study, CELL TIS RE, 299(1), 2000, pp. 81-95
Citations number
48
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cell & Developmental Biology
Journal title
CELL AND TISSUE RESEARCH
ISSN journal
0302-766X → ACNP
Volume
299
Issue
1
Year of publication
2000
Pages
81 - 95
Database
ISI
SICI code
0302-766X(200001)299:1<81:EOCRBO>2.0.ZU;2-1
Abstract
The ECL cells in the oxyntic mucosa of rat stomach produce histamine and ch romogranin A-derived peptides such as pancreastatin. The cells respond to g astrin via cholecystokinin-2 (CCK2) receptors. A CCK2 receptor blockade was induced by treatment (for up to 8 weeks) with two receptor antagonists, YM 022 and YF476. Changes in ECL-cell morphology were examined by immunocytoch emistry and electron microscopy, while changes in ECL cell-related biochemi cal parameters were monitored by measuring serum pancreastatin and oxyntic mucosal pancreastatin, and histamine concentrations, and histidine decarbox ylase (HDC) activity. The CCK2 receptor blockade reduced the ECL-cell densi ty only marginally, if at all, but transformed the ECL cells from slender, elongated cells with prominent projections to small, spherical cells withou t projections. The Golgi complex and the rough endoplasmic reticulum were d iminished. Secretory vesicles were greatly reduced in Volume density in the trans Golgi area. Circulating pancreastatin concentration and oxyntic muco sal HDC activity were lowered within a few hours. Oxyntic mucosal histamine and pancreastatin concentrations were reduced only gradually. The CCK2 rec eptor blockade was found to prevent the effects of omeprazole-evoked hyperg astrinaemia on the ECL-cell activity and density. In conclusion, gastrin, a cting on CCK2 receptors, is needed to maintain the shape, size and activity of the ECL cells, but not for maintaining the ECL-cell population.