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(Hypertension. 2000;35:758.)
© 2000 American Heart Association, Inc.

Scientific Contributions

Acute Suppression of Muscle Sympathetic Nerve Activity by Hydrocortisone in Humans

Christoph Dodt; Barbara Keyser; Matthias Mölle; Horst Lorenz Fehm; Mikael Elam

From the Department of Internal Medicine I (C.D., B.K., M.M., H.L.F.), University of Lübeck, Germany; and Institute of Clinical Neuroscience (M.E.), Department of Clinical Neurophysiology, Sahlgren Hospital, University of Gothenburg, Sweden.

Correspondence to Christoph Dodt, MD, Department of Internal Medicine, Medical University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck, Germany. E-mail dodt{at}medinf.mu-luebeck.de

Abstract—In the present study, we examined the acute influence of hydrocortisone on human sympathetic nerve activity and cardiovascular parameters. Muscle sympathetic nerve activity (MSA), heart rate, and blood pressure were monitored in 8 healthy subjects (20 to 37 years old) before and after a bolus injection of 50 mg hydrocortisone followed by a continuous infusion at 50 mg/h during a period of 3 hours in a placebo-controlled, double-blind, crossover protocol. Recordings were performed at rest and during repeated transient sympathoexcitation induced by voluntary apneas. Resting MSA and endogenous serum cortisol concentrations were also measured in a larger study group (49 experiments, 25 subjects). During the experimental period, MSA burst number increased by 56% from the control level in the placebo group. In contrast, MSA was suppressed by 25% at the end of the hydrocortisone infusion, resulting in a significant treatment effect (P<0.05). In addition, sympathoexcitation during apnea was significantly reduced with hydrocortisone after 180 minutes. In parallel with the sympathetic outflow, blood pressure decreased in the hydrocortisone-treated group, whereas it rose in the placebo group (P<0.05 between groups). No correlation was found between basal MSA and basal cortisol levels. Our results indicate that pharmacological doses of hydrocortisone acutely influence MSA responses to short- and long-lasting environmental stimuli, whereas basal native cortisol levels do not appear to be tonically involved in the regulation of resting MSA. The suppressive hydrocortisone effect is most likely induced via supraspinal autonomic centers and cannot be explained by peripheral steroid mechanisms. The effect of elevated corticosteroid levels on sympathetic nerve discharge may be an important mechanism in cardiovascular adaptations to stress.

Key Words: hormones • glucocorticoids • sympathetic nervous system

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