Circulation, Vol 88, 388-394, Copyright © 1993 by American Heart Association
U Scherrer, P Vollenweider, D Randin, E Jequier, P Nicod and L Tappy
BACKGROUND. Physiological hyperinsulinemia in lean human subjects
stimulates sympathetic nerve activity and blood flow in skeletal muscle,
but the underlying mechanism is unknown. Potential mechanisms include
central neural or peripheral actions of insulin. Glucocorticoids may
potentially interfere with both such actions and thereby may attenuate
sympathoexcitatory and vasodilatory effects of insulin in skeletal muscle.
METHODS AND RESULTS. To determine whether insulin-induced sympathetic
activation and vasodilation are attenuated by dexamethasone, we measured
muscle sympathetic nerve activity and muscle blood flow during euglycemic
hyperinsulinemia before and after short-term administration of this
pharmacological agent. Insulin concentrations, which normally doubled
sympathetic activity and markedly increased blood flow, had no such
stimulatory effect after short-term dexamethasone administration. In
contrast, responses to two noninsulin sympathetic stimuli, the Valsalva
maneuver and immersion of the hand in ice water, and the vasodilatory
response to calf vascular occlusion were not altered by dexamethasone.
CONCLUSIONS. These results demonstrate a dramatic impairment of
insulin-induced sympathetic activation and vasodilation by dexamethasone in
lean, healthy humans. This study suggests that dexamethasone administration
to lean subjects may offer an experimental model to examine underlying
mechanisms that regulate the interplay between cardiovascular, sympathetic,
and metabolic effects of insulin.
ARTICLES
Suppression of insulin-induced sympathetic activation and vasodilation by dexamethasone in humans
Department of Internal Medicine B, CHUV, Lausanne, Switzerland.
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