Adrenergic Control of Rat Gastric Somatostatin and Gastrin Release

H. Koop Division of Gastroenterology and Metabolism, Dept. of Medicine, University of Göttingen, Göttingen, FRG, and Dept. of Physiology, University of British Columbia, Vancouver, B.C., Canada

I. Behrens Division of Gastroenterology and Metabolism, Dept. of Medicine, University of Göttingen, Göttingen, FRG, and Dept. of Physiology, University of British Columbia, Vancouver, B.C., Canada

E. Bothe Division of Gastroenterology and Metabolism, Dept. of Medicine, University of Göttingen, Göttingen, FRG, and Dept. of Physiology, University of British Columbia, Vancouver, B.C., Canada

H. Koschwitz Division of Gastroenterology and Metabolism, Dept. of Medicine, University of Göttingen, Göttingen, FRG, and Dept. of Physiology, University of British Columbia, Vancouver, B.C., Canada

C. H. S. McIntosh Division of Gastroenterology and Metabolism, Dept. of Medicine, University of Göttingen, Göttingen, FRG, and Dept. of Physiology, University of British Columbia, Vancouver, B.C., Canada

R. A. Pederson Division of Gastroenterology and Metabolism, Dept. of Medicine, University of Göttingen, Göttingen, FRG, and Dept. of Physiology, University of British Columbia, Vancouver, B.C., Canada

R. Arnold Division of Gastroenterology and Metabolism, Dept. of Medicine, University of Göttingen, Göttingen, FRG, and Dept. of Physiology, University of British Columbia, Vancouver, B.C., Canada

W. Creutzfeldt Division of Gastroenterology and Metabolism, Dept. of Medicine, University of Göttingen, Göttingen, FRG, and Dept. of Physiology, University of British Columbia, Vancouver, B.C., Canada

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Abstract

The effect of adrenergic agonists and antagonists on the secretion of gastric somatostatin-like immunoreactivity (SLI) and gastrin was investigated in an isolated, vascularly perfused rat stomach preparation. Two- to six-fold increases in SLI secretion induced by isoproterenol, epinephrine, and norepinephrine were completely abolished by propranolol but were not influenced by phentolamine. Propranolol did not alter glucagon- and DB-cAMP-induced stimulation of SLI release. Experiments in which the β₂-agonist salbutamol and the β₂- and β₂-blockers practolol and H35/25 were used showed that both subtypes of β receptors are involved. Gastrin secretion revealed only minor changes in dose-response studies with a wide range of isoproterenol concentrations (2·10-⁸ to 1.5·10-⁴ M). The results obtained in this study suggest that in rats 1) the SLI response to adrenergic agonism is predominantly mediated by β receptors; 2) both β₁- and β₂-adrenergic receptors are involved; 3) under in vitro conditions, adrenergic agonism is a weak stimulus for gastrin secretion.

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Adrenergic Control of Rat Gastric Somatostatin and Gastrin Release

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Adrenergic Control of Rat Gastric Somatostatin and Gastrin Release

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