Direct neural inhibition of insulin secretion in response to systemic hypoglycemia.
The innervated pancreas of an anesthetized small "pancreas" dog was cross-perfused with blood from a large "support" dog in order to separate neural from blood-borne influences on the immunoreactive insulin secretion rate (ISR). The arterial plasma reducing sugar (sugar) concentration could be varied independently in the pancreas dog systemic circulation and in its pancreas. After tying of the hepatic arteries and portal vein in the pancreas dog, its systemic arterial plasma sugar concentration was allowed to fall in 10 experiments. This was prevented in five control experiments by intravenous glucose infusion (7 mg/kg-min). In all experiments, pancreatic arterial plasma sugar concentration was sustained, and at 40 min it was elevated 50 mg/100 ml by glucose infusion into the pancreatic blood supply. Bilateral splanchnic nerve section at 120 min caused an increase of the ISR in all experiments, but a greater rise occurred from the pancreases of the 10 dogs allowed to become hypoglycemic (P less than .02). In two further experiments, the splanchnic nerves were not cut, and no rise in ISR occurred. In conclusion, systemic hypoglycemia can inhibit insulin secretion by means of the splanchnic nerves.
D000818:Animals; D001786:Blood Glucose; D001835:Body Weight; D003427:Cross Circulation; D004285:Dogs; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D009433:Neural Inhibition; D010179:Pancreas / Q000098:blood supply / Q000294:innervation / Q000378:metabolism*; D010477:Perfusion; D012039:Regional Blood Flow; D013153:Splanchnic Nerves / Q000502:physiology* / Q000601:surgery
D001786:Blood Glucose; D007328:Insulin