Gj. Dockray et al., GASTRIN CELL RESPONSES TO ACIDIFICATION OF THE ACHLORHYDRIC RAT STOMACH, The American journal of physiology, 265(3), 1993, pp. 70000440-70000444
In the rat, gastrin cells are normally exposed to the stimulatory effe
cts of food and the inhibitory influences of acid in the gastric lumen
. We have studied the effects of intragastric acid on gastrin cell fun
ction in animals in which the tonic inhibitory action of acid was remo
ved by prior treatment with the proton pump blocker omeprazole. In fas
ted rats with gastric fistula treated with omeprazole, instillation of
acid into the stomach produced a prompt decrease in plasma gastrin, b
ut gastrin mRNA abundance showed a modest transient increase over a pe
riod of 2 h and thereafter no change; there was also a transient incre
ase in tissue concentrations of the gastrin precursor progastrin that
was compatible with increased gastrin synthesis. Concentrations of tis
sue gastrins, in general, increased after acid instillation, which can
be attributed to continued synthesis in the presence of suppressed ga
strin release. In rats fed ad libitum, a single dose of omeprazole (wh
ich produces achlorhydria for 24-30 h) produced an increase in plasma
gastrin that peaked after 24 h and declined to control levels over the
following 48 h; in contrast, gastrin mRNA abundance peaked 48 h after
omeprazole before declining to control levels. The results indicate t
hat whereas gastrin release might be promptly inhibited by intragastri
c acid, the changes in gastrin mRNA abundance are much slower: achlorh
ydria increases gastrin mRNA within 24 h, but acid takes longer to dep
ress gastrin mRNA abundance. Over periods of a few hours, gastrin rele
ase and synthesis need not, therefore, change in parallel.