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
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.