Central Nervous System-Mediated Glucagon Secretion Is Enhanced by α2-Adrenoreceptor Activation

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Abstract
We assessed the response of the adrenergic receptor in pancreatic secretion to central nervous system stimulation. Injection of neostigmine (5 .times. 10-8 mol) into the third cerebral ventricle in intact rats resulted in increased epinephrine and norepinephrine secretion associated with glucagon secretion. This glucagon secretion was still observed in bilateral adrenalectomized (ADX) rats, although its concentration was significantly lower than that in the intact rats. This glucagon rise was significantly inhibited by ip treatment of ganglionic blocker with hexamethonium. Intraperitoneal injection of .alpha.-adrenergic receptor antagonist phentolamine (5 .times. 10-7 mol), but not of .beta.-adrenergic recpetor antagonist propranolol (1 .times. 10-6 mol), reduced the hyperglucagonemic effect of a subsequent neostigmine injection in intact and ADX rats, although these antagonists did not influence epinephrine or norepinephine secretion in intact rats. In addition, ip injection of the selective .alpha.2-receptor antagonist yohimbine (5 .times. 10-7 mol), but not of the selective .alpha.1-receptor antagonist prazosin (1 .times. 10-6 mol), inhibited the neostigmine-induced glucagon secretion in intact and ADX rats. From this evidence it is suggested that central nervous system-mediated glucagon release is enhanced by .alpha.2-adrenoreceptor stimulaton by either catecholamines or the autonomic nervous system.