Sympathetic Nerve Stimulation Versus Pancreatic Norepinephrine Infusion in the Dog: 1) Effects on Basal Release of Insulin and Glucagon*

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Abstract
We investigated whether pancreatic norepinephrine (NE) infusions could reproduce the inhibition of insulin secretion and the stimulation of glucagon secretion observed during sympathetic nerve stimulation in halothane-anesthetized dogs. Three minutes of stimulating the sympathetic nerves (8 Hz, 1 msec, 10 mA, n = 6) surrounding the pancreatic artery decreased both the blood flow in the superior pancreatic vein (SPV) (.DELTA. = -1.7 .+-. 0.6 ml/min, P < 0.05) and the basal pancreatic output of immunoreactive insulin (IRI) (.DELTA. = -79 .+-. 5%, P < 0.001). SPV levels of NE increased by 683 .+-. 177 pg/ml (P < 0.02). Infusion of NE into the superior pancreatic artery at the low dose of 12 ng/min (n = 6) reproduced this increase of SPV levels of NE (.DELTA. = +740 .+-. 130 pg/ml; P < 0.01) and caused a small reduction of SPV blood flow (.DELTA. = -1.0 .+-. 0.4 ml/min, P < 0.05), but did not change pancreatic IRI (.DELTA. = -26 .+-. 16%, NS). The medium dose of NE (120 ng/min, n = 6) reproduced the nerve stimulation-induced decrease of SPV blood flow (.DELTA. = -1.5 .+-. 0.2 ml/min; P < 0.01) and increased the SPV NE levels by 6,306 .+-. 1,839 pg/ml (P < 0.02), yet did not decrease pancreatic IRI output (.DELTA. = +62 .+-. 49%, NS). The high dose of NE (1,200 ng/min, n = 6) produced an extreme increment of SPV NE levels (.DELTA. = +180,000 .+-. 44,000 pg/ml, P < 0.001) and a much larger reduction of SPV blood flow (.DELTA. = -3.7 .+-. 0.7 ml/min, P < 0.01) than did nerve stimulation, yet still did not inhibit insulin output (.DELTA. = -13 .+-. 46%, NS). Ten minutes of sympathetic nerve stimulation increased the pancreatic output of immunoreactive glucagon (IRG) by 1435 .+-. 419 pg/min (P < 0.02). Pancreatic IRG output increased as well during infusion of NE for 10 min at both 12 ng/min (by 575 .+-. 205 pg/min, P < 0.05) and 120 ng/min (by 718 .+-. 231 pg/min, P < 0.05). In marked contrast, during infusion of NE at 1200 ng/min, pancreatic IRG output decreased (by 400 .+-. 190 pg/min, P < 0.05). We conclude: (1) that selective electrical stimulation of the sympathetic nerves entering the pancreas decreases pancreatic blood flow, inhibits basal IRI output, and stimulates basal IRG output; (2) that moderate rates of local NE infusions also decrease pancreatic venous blood flow and stimulate basal IRG output yet do not inhibit pancreatic IRI output. These results suggest that the stimulation of glucagon secretion during sympathetic nerve stimulation is partially mediated by NE whereas the inhibition of insulin secretion is not.