RENIN AS A BIOLOGICAL MARKER OF THE NREM-REM SLEEP CYCLE - EFFECT OF REM-SLEEP SUPPRESSION

We have previously described that, in normal man, the nocturnal oscill ations of plasma renin activity (PRA) exactly reflect the rapid eye mo vement (REM)-non(N)REM sleep cycles, with increasing PRA levels during NREM sleep and decreasing levels during REM sleep. This study was car ried out to determine whether REM sleep suppression affects nocturnal renin profiles and to define which sleep stage is essential for renin release. In a first experimental series, REM sleep was suppressed by u sing clomipramine, a tricyclic antidepressant. Seven healthy young men were studied once during a night when a placebo was given and once du ring a night following a single dose of 50 mg clomipramine. Blood was collected every 10 min from 23.00 hours to 07.00 hours. PRA was measur ed by radio-immunoassay and the nocturnal profiles were analysed using the pulse detection program ULTRA. Clomipramine suppressed REM sleep in all subjects but one, but did not affect the number of SWS episodes nor their duration. Similar PRA profiles were observed in both experi mental conditions. Neither the mean levels, nor the number and the amp litude of the oscillations were modified and the normal relationship b etween slow wave sleep and increasing PRA levels was preserved. In a s econd experimental series, REM sleep was prevented by rapidly awakenin g the subjects as soon as they fell into REM sleep. The four subjects studied attempted several times to go into REM sleep, but only when PR A levels were decreasing. The interruption of REM sleep by short wakin g periods did not disturb PRA for which the oscillations remained unaf fected. Again, the relationship between SWS and increasing PRA levels was preserved. These results provide evidence that mechanisms increasi ng slow-wave activity are principally involved in increasing PRA level s and that replacing REM sleep by waking periods and light sleep does not modify nocturnal PRA oscillations.