Adrenergic Modulation of Pancreatic A, B, and D Cells

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Abstract
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.
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