Pharmacopsychiatry · 2006
Renin-angiotensin-aldosterone system, HPA-axis and sleep-EEG changes in unmedicated patients with depression after total sleep deprivation.
Клиническое исследованиеСтатьяНазвание и аннотация: Перевод в очереди
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Murck H, Uhr M, Ziegenbein M, Künzel H, Held K, Antonijevic I A, Schüssler P, Steiger A
Аннотация
BACKGROUND: Changes in the activity of the renin-angiontensin-aldosterone system (RAAS) in depression have recently been reported. Renin and aldosterone secretion are coupled to sleep in healthy subjects. As total sleep deprivation (TSD) leads to a rapid mood improvement in patients with depression, it is of interest to investigate its effect on the response of the RAAS in the recovery night in this population as a possible probe for the neurobiological effects of TSD and potentially other rapid acting antidepressive interventions. Additionally we explored the HPA-system and the sleep-EEG-changes.
METHODS: We compared the sleep related activity of the RAAS before and after TSD in seven depressed patients. After an accommodation night, a polysomnographic examination was performed between 23.00 h and 7.00 h. This was followed by 40 h of TSD and a second polysomnography. During the examination blood samples were taken in the night every 20 min for analysis of renin, aldosterone, ACTH and cortisol.
RESULTS: During recovery-sleep renin was significantly increased (p < 0.05). Aldosterone showed no change. ACTH and cortisol were decreased by trend in the first half of the night. REM-density and intermittent wakefulness was significantly decreased (p < 0.05), whereas slow wave sleep increased by trend in the first half of the night.
CONCLUSION: TSD in patients with depression leads to an increase in renin secretion and a concomitant trend for a decrease in HPA axis activity in the recovery night. These changes could be a "fingerprint" of a rapidly antidepressive treatment.
METHODS: We compared the sleep related activity of the RAAS before and after TSD in seven depressed patients. After an accommodation night, a polysomnographic examination was performed between 23.00 h and 7.00 h. This was followed by 40 h of TSD and a second polysomnography. During the examination blood samples were taken in the night every 20 min for analysis of renin, aldosterone, ACTH and cortisol.
RESULTS: During recovery-sleep renin was significantly increased (p < 0.05). Aldosterone showed no change. ACTH and cortisol were decreased by trend in the first half of the night. REM-density and intermittent wakefulness was significantly decreased (p < 0.05), whereas slow wave sleep increased by trend in the first half of the night.
CONCLUSION: TSD in patients with depression leads to an increase in renin secretion and a concomitant trend for a decrease in HPA axis activity in the recovery night. These changes could be a "fingerprint" of a rapidly antidepressive treatment.