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Glucocorticoids, sympathetic activity, and presynaptic alpha 2-adrenoceptor function in humans
J W Lenders1, A Golczynska, D S Goldstein
1Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA.
The Journal of Clinical Endocrinology and Metabolism
|June 1, 1995
Summary
Glucocorticoids, like prednisone, reduce sympathetic nervous system activity and norepinephrine levels in humans. This sympathoinhibition occurs independently of alpha 2-adrenoceptor function, indicating a direct effect on sympathetic outflow.
Area of Science:
- Neuroendocrinology
- Autonomic Neuroscience
Background:
- The sympathetic nervous system and pituitary-adrenocortical system are key stress response pathways.
- Animal studies suggest glucocorticoids inhibit sympathetic activity and alpha 2-adrenoceptor function.
Purpose of the Study:
- To investigate the effects of glucocorticoids on sympathetic outflow and alpha 2-adrenoceptor modulation in humans.
- To determine if prednisone influences norepinephrine release and sympathetic nerve activity.
Main Methods:
- A randomized, double-blind, placebo-controlled crossover study involving 15 healthy subjects.
- Administration of prednisone (20 mg daily) or placebo for one week, followed by washout and crossover.
- Measurement of plasma catecholamines and ACTH, and peroneal muscle sympathetic nerve activity (MSNA) before and after yohimbine challenge.
Main Results:
- Prednisone significantly decreased plasma norepinephrine (NE) levels and MSNA compared to placebo.
- Yohimbine (YOH) increased blood pressure and heart rate, with prednisone not altering these responses.
- Prednisone did not affect YOH-induced increases in NE or MSNA, suggesting an effect independent of alpha 2-adrenoceptors.
Conclusions:
- Glucocorticoids inhibit sympathoneural outflow in humans.
- The observed sympathoinhibition by glucocorticoids is independent of altered alpha 2-adrenoceptor modulation of noradrenergic terminals.