Hyperinsulinemia produces cardiac vagal withdrawal and nonuniform sympathetic activation in normal subjects

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology Vol. 276; no. 1; pp. 178 - R183
• Main Authors: Van De Borne, Philippe, Hausberg, Martin, Hoffman, Robert P, Mark, Allyn L, Anderson, Erling A
• Format: Journal Article
• Language: English
• Published: United States 01.01.1999
• Subjects: Adrenergic beta-Antagonists - pharmacology; Adult; Female; Glucose Clamp Technique; Heart Conduction System - physiopathology; Heart Rate - drug effects; Humans; Hyperinsulinism - physiopathology; Infusions, Intravenous; Male; Pharmaceutical Vehicles - pharmacology; Propranolol - pharmacology; Reference Values; Sympathetic Nervous System - physiopathology; Vagus Nerve - physiopathology
• ISSN: 0363-6119; 0002-9513; 1522-1490
• DOI: 10.1152/ajpregu.1999.276.1.r178

Departments of 1  Internal Medicine, 2  Pediatrics, and 3  Anesthesia, Cardiovascular and Clinical Research Centers, University of Iowa College of Medicine and Veterans Affairs Medical Center, Iowa City, Iowa 52242 The exact mechanisms for the decrease in R-R interval (RRI) during acute physiological hyperinsulinemia with euglycemia are unknown. Power spectral analysis of RRI and microneurographic recordings of muscle sympathetic nerve activity (MSNA) in 16 normal subjects provided markers of autonomic control during 90-min hyperinsulinemic/euglycemic clamps. By infusing propranolol and insulin ( n  = 6 subjects), we also explored the contribution of heightened cardiac sympathetic activity to the insulin-induced decrease in RRI. Slight decreases in RRI ( P  < 0.001) induced by sevenfold increases in plasma insulin could not be suppressed by propranolol. Insulin increased MSNA by more than twofold ( P  < 0.001), decreased the high-frequency variability of RRI ( P  < 0.01), but did not affect the absolute low-frequency variability of RRI. These results suggest that reductions in cardiac vagal tone and modulation contribute at least in part to the reduction in RRI during hyperinsulinemia. Moreover, more than twofold increases in MSNA occurring concurrently with a slight and not purely sympathetically mediated tachycardia suggest regionally nonuniform increases in sympathetic activity during hyperinsulinemia in humans. insulin; muscle sympathetic nerve activity