In order to characterize the adrenergic control of the pancreatic A cell the effect on glucagon secretion of three sympathomimetic substances - epinephrine, isoproterenol and phenylephrine - and two adrenergic blocking agents - propranolol and phentolamine - were tested separately in the basal state and during glucagon hypersecretion induced by arginine infusion or glucopenia, using the isolated perfused rat pancreas. Epinephrine and isoproterenol infusion caused a prompt and sustained glucagon release in the basal state and potentiated glucagon response to metabolic stimuli. Insulin secretion was suppressed by epinephrine and slightly stimulated by isoproterenol. The stimulatory effect on glucagon secretion observed during phenylephrine infusion was abolished by concomitant propranolol infusion and potentiated by phentolamine. Insulin secretion was markedly depressed by phenylephrine: this effect was reserved by concomitant phentolamine infusion, while no effect was observed by concomitant propranolol infusion. Propranolol caused a suppression of both glucagon and insulin secretion, while phentolamine slightly enhanced glucagon and insulin production. In conclusion, beta-adrenergic receptor stimulation markedly increased pancreatic glucagon secretion and slightly enhanced pancreatic beta-cell activity; conversely, alpha-adrenergic agents markedly depressed insulin secretion while scarcely influencing glucagon production.
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