Glucocorticoid-induced sympathoinhibition in humans

To test whether glucocorticoids inhibit sympathetic nerve activity or norepinephrine release in humans, as has been suggested by results in laboratory animals.

This was a double-blind, placebo-controlled, randomized crossover study performed at the Clinical Center of the National Institutes of Health. Thirteen normal volunteers received 20 mg prednisone or placebo orally each morning for 1 week, followed by a washout period of 1 week and then by treatment with the other drug for 1 week. On the last day of each treatment week, blood samples were drawn for measurements of plasma levels of catecholamines and their metabolites, of cortisol, and of corticotropin at baseline and during reflexive sympathetic stimulation elicited by lower body negative pressure (-15 mm Hg). A 24-hour urine collection was obtained at the end of each week of treatment for measurement of urinary excretion of catechols. In eight subjects, directly recorded peroneal skeletal muscle sympathetic nerve activity was also measured after both treatments.

Prednisone significantly decreased sympathetic nerve activity by 23% +/- 6%, plasma norepinephrine levels by 27% +/- 6%, and plasma corticotropin levels by 77%. Blood pressure, heart rate, body weight, and urinary excretion of catechols and electrolytes were unaffected. Prednisone did not alter proportionate increments in sympathetic nerve activity or plasma norepinephrine levels during lower body negative pressure. Relationships between sympathetic nerve activity and plasma norepinephrine levels were unchanged.

Glucocorticoids decrease sympathoneural outflows in humans without affecting acute sympathoneural responses to decreased cardiac filling and probably without affecting presynaptic modulation of norepinephrine release.