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1 Division of Endocrinology, Diabetes and Hypertension and the Clinical Research Center, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA
2 Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, MA, USA
* To whom correspondence should be addressed. E-mail: hurwitz{at}hms.harvard.edu.
Exposure to prolonged bedrest is known to induce changes in the renin angiotensin aldosterone system (RAAS) by way of posture, sodium and potassium balance, and stress, which may have serious consequences for patients. We focused on the diurnal variation of the RAAS by investigating changes in the levels of plasma renin activity (PRA) and aldosterone; for comparison to markers of the intrinsic pacemaker and to stress, we measured melatonin and cortisol. PRA, aldosterone, melatonin, and cortisol were measured hourly in 10 normal subjects with standardized sleep patterns, posture, and diet at baseline and after 11 days of prolonged bedrest conducted under a light-dark cycle. Circadian characteristics of hormone secretion patterns were estimated by multiple harmonic regression with excellent goodness-of-fit measures. Variability in the melatonin and cortisol patterns across subjects was minimal. Even for pulsatile hormones, this technique successfully estimated the acrophase, which was the salient feature. Baseline hormone peak times started with melatonin near the middle of the sleep period, followed by PRA, then aldosterone, and then cortisol around wake time. Prolonged bedrest did not induce significant changes in any timing characteristic of the secretion patterns. Baseline and prolonged bedrest peak times for melatonin and cortisol and amplitude characteristics for all hormones were highly correlated, indicating consistency within individuals. These data provide strong evidence that prolonged bedrest of 11 days duration does not disrupt either the timing characteristics of the RAAS or the intrinsic pacemaker.
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