Hyperglycemia without hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans

To explore the effects of the acute induction of hyperglycemia on sympathetic activity and vascular function we studied eight normal control subjects (28 +/- 3 years of age). Muscle sympathetic nerve activity (MSNA) and forearm vascular resistance (FVR) were measured before (5.4 +/- 0.2 mmol/L) and during systemic infusion of 20% dextrose with octreotide (250 microg/h) and low dose insulin (4 mU x m(-2) x min(-1)) with 60 min of hyperglycemia (venous plasma glucose, 12.5 +/- 0.6 mmol/L). To control for the effects of hyperosmolarity and volume infusion subjects returned for two control studies with equal volume 20% mannitol and 0.2% saline infusions instead of dextrose infusion. The increase in MSNA during hyperglycemia (178 +/- 48 units) was significantly greater than the increase during mannitol (69 +/- 46 units, p < 0.001) or during 0.2% saline (28 +/- 28 units, p < 0.001). The decreases in FVR after 60 min of hyperglycemia (20 +/- 4 units, p = 0.002) and mannitol (13 +/- 4 units, p = 0.033) were significantly greater than the decrease during saline (0.1 +/- 4 units). The changes in FVR during hyperglycemia and mannitol did not differ. Acute hyperglycemia causes sympathoexcitation and peripheral vasodilation. The vascular effect may be mediated by increased osmolar load.