INTERLEUKIN-1-BETA INHIBITS GASTRIC HISTAMINE-SECRETION AND SYNTHESIS IN THE RAT

被引：60

作者：

KONDO, S ^{[1
]}

SHINOMURA, Y ^{[1
]}

KANAYAMA, S ^{[1
]}

KAWABATA, S ^{[1
]}

MIYAZAKI, Y ^{[1
]}

IMAMURA, I ^{[1
]}

FUKUI, H ^{[1
]}

MATSUZAWA, Y ^{[1
]}

机构：

[1] OSAKA UNIV, SCH MED, DEPT PHARMACOL 2, SUITA, OSAKA 565, JAPAN

来源：

AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY | 1994年 / 267卷 / 06期

关键词：

GASTRIC ACID SECRETION; HISTIDINE DECARBOXYLASE; URINARY HISTAMINE EXCRETION; PROSTAGLANDINS;

D O I：

10.1152/ajpgi.1994.267.6.G966

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

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 mu g/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 mu g/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.

引用

页码：G966 / G971

页数：6

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