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  • Title: Adrenergic modulation of pancreatic A, B, and D cells alpha-Adrenergic suppression and beta-adrenergic stimulation of somatostatin secretion, alpha-adrenergic stimulation of glucagon secretion in the perfused dog pancreas.
    Author: Samols E, Weir GC.
    Journal: J Clin Invest; 1979 Feb; 63(2):230-8. PubMed ID: 34627.
    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 beta-receptor blockade was tested, and putative alpha-adrenergic effects were confirmed by combined alpha- and beta-adrenergic receptor blockade.beta-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.alpha-Adrenergic agonism (10 ng/ml epinephrine) after beta-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 beta-adrenergic blockade. The alpha-adrenergic effects on the D and A cell were abolished by either phentolamine or by phenoxybenzamine. This study showed that there are indeed alpha-adrenergic receptors on A cells and that the secretion of glucagon, a "stress" hormone, was stimulated either by alpha- or beta-adrenergic receptor agonism. D-cell secretion, like that of the B cell, was inhibited by alpha-adrenergic agonism and was stimulated by beta-adrenergic agonism. However, beta-adrenergic-induced changes in D-cell secretion were smaller in magnitude than those of B-cell secretion.
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