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

Citation
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
Citations number
24
Categorie Soggetti
Endocrynology, Metabolism & Nutrition
Journal title
JOURNAL OF DIABETES AND ITS COMPLICATIONS
ISSN journal
10568727 → ACNP
Volume
13
Issue
1
Year of publication
1999
Pages
17 - 22
Database
ISI
SICI code
1056-8727(199901/02)13:1<17:HWHPBS>2.0.ZU;2-B
Abstract
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.