Bombesin Inhibits Histamine Release from the Rat Oxyntic Mucosa by a Somatostatin-dependent Mechanism

A. K. Sandvik Physiological Laboratory and Institute of Cancer Research, University School of Medicine, Trondheim, Norway; Dept. of Medical Physiology, The Panura Institute, University of Copenhagen, Copenhagen, Denmark

E. Brenna Physiological Laboratory and Institute of Cancer Research, University School of Medicine, Trondheim, Norway; Dept. of Medical Physiology, The Panura Institute, University of Copenhagen, Copenhagen, Denmark

A. Sundan Physiological Laboratory and Institute of Cancer Research, University School of Medicine, Trondheim, Norway; Dept. of Medical Physiology, The Panura Institute, University of Copenhagen, Copenhagen, Denmark

J. J. Holst Physiological Laboratory and Institute of Cancer Research, University School of Medicine, Trondheim, Norway; Dept. of Medical Physiology, The Panura Institute, University of Copenhagen, Copenhagen, Denmark

H. L. Waldum Physiological Laboratory and Institute of Cancer Research, University School of Medicine, Trondheim, Norway; Dept. of Medical Physiology, The Panura Institute, University of Copenhagen, Copenhagen, Denmark

Abstract

Background and methods: This study examines the effect of bombesin on endogenous somatostatin and the histamine-synthesizing enterochromaffin-like cells. Somatostatin and histamine were measured in the venous effluent of isolated/antrectomized vascularly perfused rat stomachs after administration of bombesin and gastrin alone or combined. Histidine decarboxylase (HDC) enzyme activity and mRNA abundance were measured in the gastric corpus after intravenous administration of bombesin to conscious rats. Results: Bombesin released somatostatin from the isolated stomachs and reduced basal and gastrin-stimulated venous histamine. Somatostatin antiserum partially reversed the effect of bombesin on basal and gastrin-stimulated histamine release. In conscious fed rats, intravenous bombesin doubled serum gastrin concentrations and increased HDC activity. Conclusion: We conclude that endogenous (paracrine) somatostatin inhibits basal and gastrin-stimulated histamine release from the ECL cell. In intact animals this effect is surmountable by simultaneously released gastrin, suggesting that a balance between the effects of gastrin and somatostatin determines the activation of the ECL cell.

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Bombesin Inhibits Histamine Release from the Rat Oxyntic Mucosa by a Somatostatin-dependent Mechanism

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Bombesin Inhibits Histamine Release from the Rat Oxyntic Mucosa by a Somatostatin-dependent Mechanism

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