Gluco- and antimineralocorticoid effects on human sleep: a role of central corticosteroid receptors

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Abstract
Cortisol modulates brain functions in humans. This principal endogenous glucocorticoid in humans decreases rapid-eye-movement (REM) sleep and increases slow-wave sleep (SWS). Because cortisol exerts its effect on brain functions via mineralocorticoid receptors (MR) and glucocorticoid receptors (GR), we were interested in which type of corticosteroid receptor mediates these steroid effects on sleep. Healthy men were tested in two double-blind experiments. In experiment I (n = 8), the subject's sleep was tested during four nights: 1) after pretreatment with dexamethasone (Dex, 4 mg/day) for 4 or 6 days and after additional infusion of placebo or cortisol (10 mg/h) during the experimental night, 2) after pretreatment with placebo for 4 or 6 days and after infusion of placebo or cortisol (10 mg/h) during the experimental night. In experiment II, subjects (n = 10) slept after intravenous administration of potassium canrenoate (200 mg, at 0800 and 1700 h before experimental nights) or placebo. Cortisol infusion moderately increased the percentage of SWS (P less than 0.05) and markedly decreased REM sleep (P less than 0.01); influence of cortisol on SWS did not depend on pretreatment with Dex. Dex reduced both SWS and REM sleep (P less than 0.05). Canrenoate markedly diminished SWS (P less than 0.01) but left REM sleep unaffected. The results suggest that corticosteroid-induced changes in SWS are mediated via MR-like central receptors in humans, whereas changes in REM sleep involve GR.