AJP - Endocrinology and Metabolism, Vol 263, Issue 5 E935-E942, Copyright © 1992 by American Physiological Society
Hypertension and insulin resistance: role of sympathetic nervous system activity
M. A. Supiano, R. V. Hogikyan, L. A. Morrow, F. J. Ortiz-Alonso, W. H. Herman, R. N. Bergman and J. B. Halter
Department of Internal Medicine, University of Michigan, Ann Arbor 48109.
The purpose of this study was to test the hypothesis that heightened
sympathetic nervous system (SNS) activity contributes to the mechanism by
which hypertension is associated with insulin resistance in humans. We
performed frequently sampled intravenous glucose tolerance tests to
determine tissue sensitivity to metabolic effects of insulin (SI) and
measured plasma norepinephrine (NE) levels in 21 normotensive and 14
hypertensive Caucasian subjects. Compared with the normotensive subjects,
hypertensive subjects had decreased SI (5.4 +/- 0.5 vs. 4.0 +/- 0.7 x
10(-5) x min-1 x pM-1; P = 0.03) but similar plasma NE levels
(normotensive: 1.82 +/- 0.12 vs. hypertensive: 1.73 +/- 0.16 nM; P = 0.23).
In a multiple regression model, only body mass index (BMI) and mean
arterial blood pressure (MABP) were significant independent predictors of
SI [SI = (-0.513)(BMI) + (-0.058)(MABP) + 23.6; r = 0.748; P = 0.0001];
age, plasma glucose, epinephrine, and NE level did not enter this model. As
an additional test of this hypothesis, seven hypertensive subjects were
restudied after 10 days of guanadrel therapy to determine whether SI would
increase during suppression of SNS activity by guanadrel. Despite a
significant reduction in plasma NE levels with guanadrel (baseline: 1.63
+/- 0.18 vs. guanadrel: 0.99 +/- 0.14 nM; P = 0.01), there was no
significant change in SI (baseline: 2.97 +/- 0.78 vs. guanadrel: 2.41 +/-
0.54 x 10(-5).min-1 x pM-1; analysis of variance P = 0.57). We conclude
that, in the Caucasian population we studied, heightened SNS activity is
not essential for the insulin resistance observed in hypertensive humans.
