Oral E2 prostaglandins affect endocrine cell populations in the gastric antrum of the rat

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Abstract
The aim of the present study was to investigate antral endocrine cell populations and tissue and circulating hormone levels following a 4-week oral regimen with prostaglandin E2 (25, 250 and 5000 .mu.g kg-1 b.i.d.) or a stable methyl analogue (5 and 50 .mu.g kg-1 b.i.d.). Epithelial hyperplasia of the gastric antrum was observed with the highest dose of prostaglandin E2 and both doses of the analogue, as evaluated by stereological methods and conventional cell count. The treatments significantly affected the endocrine cell population. Somatostatin-immunoreactive cells were increased in proportion to the increased epithelial cellularity and plasma levels of somatostatin were increased in parallel. The tissue content of somatostatin-like immunoreactivity differed according to the extraction procedure used, and was significntly higher than controls in specimens extracted in neutral water. In the neutral extracts of immunoreactive somatostatin of unidentified molecular structure dominated quantitatively over somatostatin 14 and 28, which were the major components in acetic acid extracts. The serotonin-immunoreactive cell population was also significantly increased by natural prostaglandin E2 and the analogue but the gastrin cell population was not significantly affected by treatments. Accordingly, no significant changes were observed in tissue or plasma gastrin levels. It is concluded that the epithelial hyperplasia of the antral epithelia produced by E2 prostaglandins is associated with selective changes of endocrine cell populations. The changes were proportional to the increaes of epithelial cellularity and required quantitative determination of the total antral volume to be detected. It may seem surprising that the most consistent finding in the hyperplastic antral mucosa was an increase of somatostatin-immunoreactive cell population, and elevated tissue and plasma concentrations of this peptide, which has anti-trophic actions on gastrointestinal epithelia. It is possible that somatostatin increments contribute to restrict the hyperplasia and are responsible for the reduced new cell production observed in prostaglandin-induced hyperplasia of gastric and intestinal epithelia.