Adrenergic Control of Rat Gastric Somatostatin and Gastrin Release

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 6-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[dibutyryl]-cAMP-induced stimulation of SLI release. Experiments in which the .beta.2-agonist salbutamol and the .beta.1- and .beta.2-blockers practolol and H35/25 [.alpha.-4-dimethyl-N-isopropyl phenylethanolamine] were used, showed that both subtypes of .beta. receptors are involved. Gastrin secretion revealed only minor changes in dose-response studies with a wide range of isoproterenol concentrations (2 .cntdot. 10-8 to 1.5 .cntdot. 10-4 M). In rats the SLI response to adrenergic agonism is probably predominantly mediated by .beta. receptors; both .beta.1- and .beta.2-adrenergic receptors are apparently involved, and under in vitro conditions, adrenergic agonism may be a weak stimulus for gastrin secretion.