Bilateral carotid occlusion and the sympathetic regulation of insulin secretion.

After a 2-min bilateral carotid arterial occlusion (BCO) in puppies, a centrally originating, sympathetic discharge takes place which increases heart rate and blood pressure. We examined the specificity of this sympathetic neural outflow by determining whether it also caused a direct neurally mediated inhibition of insulin release from the pancreas. The effects of this BCO on portal venous insulin concentrations, as well as on heart rate and blood pressure, were examined during i.v. glucose infusions of 0 (saline), 5 and 15 mg/kg X min-1. To determine changes in splanchnic blood flow and to more closely estimate pancreatic insulin secretion rates, a major vein draining the pancreas, the gastroduodenal, was catheterized. Blood flows and the amount of insulin traversing this vein per min (insulin flow rate) were followed before, during and after BCO. BCO decreased portal vein insulin concentrations during i.v. glucose infusions of 5 and 15 mg/kg X min-1, but not when saline was infused. Since bilateral splanchnicotomy altered this result little and since BCO increased blood flow and the insulin flow rate in the gastroduodenal vein, it appears that the lower portal venous insulin concentrations during BCO are secondary, not to sympathetically induced decrease in insulin secretion rates but, to dilution of pancreatic effluent blood. We conclude that while BCO causes appropriate changes in heart rate and blood pressure, this central stimulus to the sympathetic system does not provide a direct neuroendocrine reflex change in insulin secretion. BCO alters portal venous insulin concentration indirectly, and the alteration depends on the plasma glucose concentration and an enhancement in the splanchnic blood flow.