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Free access | 10.1172/JCI109294
The Veterans Administration Medical Center, University of Louisville School of Medicine, Louisville, Kentucky 40202
Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky 40202
Department of Medicine, Medical College of Virginia, Richmond, Virginia 23298
Find articles by Samols, E. in: JCI | PubMed | Google Scholar
The Veterans Administration Medical Center, University of Louisville School of Medicine, Louisville, Kentucky 40202
Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky 40202
Department of Medicine, Medical College of Virginia, Richmond, Virginia 23298
Find articles by Weir, G. in: JCI | PubMed | Google Scholar
Published February 1, 1979 - More info
The effects of adrenergic substances on pancreatic insular secretions were studied in a completely isolated canine pancreas with exclusion of the duodenum from the perfusion circuit. To ensure adequate blockade, blockers were infused before agonists. A dose range of β-receptor blockade was tested, and putative α-adrenergic effects were confirmed by combined α- and β-adrenergic receptor blockade.
β-Adrenergic agonism (2 ng/ml isoproterenol) induced a mean integrated increase of 79±20% in somatostatin secretion, whereas glucagon and insulin secretion were increased by 185±45 and 495±146%, respectively. The stimulations of D, A, and B cells were abolished by propranolol.
α-Adrenergic agonism (10 ng/ml epinephrine) after β-adrenergic blockade) moderately decreased somatostatin (−37±7%) secretion, moderately increased glucagon (91±19%), and markedly decreased insulin (−85±3%) release. Similar effects on D-, A-, and B-cell secretion were induced with 2 ng/ml epinephrine or 10 ng/ml norepinephrine after β-adrenergic blockade. The α-adrenergic effects on the D and A cell were abolished by either phentolamine or by phenoxybenzamine.
This study showed that there are indeed α-adrenergic receptors on A cells and that the secretion of glucagon, a “stress” hormone, was stimulated either by α- or β-adrenergic receptor agonism. D-cell secretion, like that of the B cell, was inhibited by α-adrenergic agonism and was stimulated by β-adrenergic agonism. However, β-adrenergic-induced changes in D-cell secretion were smaller in magnitude than those of B-cell secretion.