Neural Release of Glucagon Is Inhibited by Hyperglycemia and Enhanced by Phentolamine

Using an innervated, cross-perfused, canine pancreasstomach–duodenum preparation, direct neural effects on the immunoreactive glucagon secretion rate (GSR) were separated from bloodborne influences. Both splanchnic nerves were cut above the diaphragm and stimulated simultaneously for three separate 10-min-long periods, twice before and once during a pancreatic arterial phentolamine infusion. The extent of the decrease in GSR that occurred after nerve section was inversely correlated with the arterial plasma glucose concentration at the time of section. Splanchnic nerve stimulation caused a significant increase in GSR. Similar stimulation during a pancreatic arterial phentolamine infusion caused a significantly greater increase. Rapid infusion of glucose near the end of the experiment caused a significant decrease in GSR, demonstrating the responsiveness of the preparation. These data were collected in conjunction with a study of neural influences on insulin secretion rates.² It can be concluded that the central nervous system can alter the secretion rate of glucagon by direct neural means. Alpha-adrenergic blockade, in the presence of splanchnic nerve stimulation, enhances GSR.