AIM: To investigate the effect of centrally administered
oxytocin and its receptor antagonist, atosiban, on gasuic
acid secretion and on experimentally induced gastric and
duodenal ulcers. METHODS: The acute gastric ulcer
models, such as pylorus ligation, indomethacin-induced
and ethanol-induced gastric ulcers were used. Chronic
gastric ulcers were induced by acetic acid and duodenal
ulcers by cysteamine HC1. RESULTS: In pylorus
ligated rats, oxytocin ( 10 μg/kg, icv) showed signifi
cant antisecretory and antiulcer activity (P<0.01 ).
However, it aggravated the ethanol-induced gastric ulcers
and did not show any effect on indomethacin-induced gas
tric ulcers. Oxytocin increased gastric ulcer healing in
acetic acid-induced chronic gastric ulcers. The effect of
oxytocin was reversed by atosiban (10 μg/kg, icy), a
selective oxytocin receptor antagonist. Atosiban when
given alone increased gastric acid secretion and ulcer
index in pylorus-ligated rats and also aggravated acetic
acid-induced chronic gastric ulcers. It seems the antiul
cer activity of oxytocin was due to its anti-secretory ef
fect. CONCLUSION: Centrally administered oxytocin
possesses gastric anti-secretory and anti-ulcer activity and
oxytocin antagonist, atosiban, is pro-ulcerogenic in rats.