Rp. Hoffman et al., Hyperglycemia without hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans, J DIABET C, 13(1), 1999, pp. 17-22
To explore the effects of the acute induction of hyperglycemia on sympathet
ic activity and vascular function we studied eight normal control subjects
(28 +/- 3 years of age). Muscle sympathetic nerve activity (MSNA) and forea
rm vascular resistance (FVR) were measured before (5.4 +/- 0.2 mmol/L) and
during systemic infusion of 20% dextrose with octreotide (250 mu g/h) and l
ow dose insulin (4 mU.m(-2).min(-1)) with 60 min of hyperglycemia (venous p
lasma glucose, 12.5 +/- 0.6 mmol/L). To control for the effects of hyperosm
olarity and volume infusion subjects returned for two control studies with
equal volume 20% mannitol and 0.2% saline infusions instead of dextrose inf
usion. The increase in MSNA during hyperglycemia (178 +/- 48 units) was sig
nificantly 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 d
uring 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. (C) 1999 Elsevier Science Inc.