Interleukin-1 beta (IL-1 beta) is the most potent inhibitor of gastric acid secretion known at present. Although
histamine has been shown to be an important mediator of gastric acid secretion, the effect of
IL-1 beta on gastric
histamine mobilization has not been studied. In the present study, the effects of
IL-1 beta on gastric acid secretion and gastric
histamine mobilization were investigated in conscious rats with both gastric and
vesical fistulas.
IL-1 beta (5 micrograms/kg iv) significantly inhibited basal
acid secretion but did not affect basal urinary
histamine excretion and fundic
histidine decarboxylase (HDC) activity. Gastrin-17-I (1 nmol.kg-1.h-1) caused a marked increase in
acid secretion, urinary
histamine secretion, and fundic HDC activity.
IL-1 beta (5 micrograms/kg iv) completely inhibited
gastrin-induced
acid secretion and partially inhibited urinary
histamine excretion and fundic HDC activity. Pretreatment with
indomethacin (10 mg/kg ip) partially reversed the inhibitory effects of
IL-1 beta on
gastrin-stimulated fundic HDC activity and
acid secretion. These findings indicate that
IL-1 beta inhibits gastric
histamine mobilization through both
prostaglandin-dependent and
prostaglandin-independent pathways. Furthermore, it is suggested that the inhibitory action of
IL-1 beta on gastric acid secretion is mediated by the inhibition of gastric
histamine mobilization.