Hypertension, Vol 23, 1006-1011, Copyright © 1994 by American Heart Association
KA Jamerson, SD Smith, JV Amerena, E Grant and S Julius
We used the insulin-perfused human forearm model to assess the effects of
vasoconstriction induced with norepinephrine on the extraction of glucose
in the forearm in two groups of healthy young volunteers. The
norepinephrine findings were compared with a previously studied group in
which vasoconstriction has been caused by reflex activation of the
sympathetic nervous system. The aim of the study was to determine the
relative importance of hemodynamic and receptor-mediated mechanisms of
insulin resistance. Plasma insulin, arterial and venous glucose samples,
and forearm blood flow were measured at 10-minute intervals during a
30-minute baseline, a 60-minute intra-arterial insulin infusion, and during
30 minutes of insulin infusion plus vasoconstriction. Group 1 (n = 14) had
physiological vasoconstriction induced by inflation of bilateral thigh
cuffs to 40 mm Hg to cause pooling of blood in the lower extremities and
reflex vasoconstriction in the forearm; group 2 (n = 8) had intra-arterial
infusion of norepinephrine to achieve the same degree of vasoconstriction
as seen with inflation of thigh cuffs in group 1. Subjects in group 3 (n =
7) had infusion of intra-arterial norepinephrine to achieve a twofold
increase in physiological vasoconstriction. With a physiological decrease
in forearm blood flow (group 1), there was a 19% decrease in forearm blood
flow resulting in a 23% reduction in glucose uptake in the forearm (P <
.03). The same degree of reduction in forearm blood flow with a
predominantly alpha-adrenergic agonist, norepinephrine (group 2), causes
much less insulin resistance (a decrease in utilization of 13%) (P <
.04).(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Vasoconstriction with norepinephrine causes less forearm insulin resistance than a reflex sympathetic vasoconstriction
Department of Internal Medicine, University of Michigan Medical School, Ann Arbor 48109-0356.
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