Mounting epidemiological evidence links short sleep with an increase in hypertension of 60% or more, and a strong relationship has been reported between cardiovascular disease and short sleep. However, the research regarding the renal system's role on the relation between sleep deprivation/circadian disruption and hypertension is sparse. We hypothesize that sleep deprivation is causally related to the elevation of blood pressure, through the involvement of RAAS upregulation and increased markers of impaired renal function. To test our hypothesis, we will examine the RAAS and renal biomarkers in two completed sleep deprivation studies. In study 1, 24 participants completed a 7-day in-hospital study. After two baseline days, participants were randomly assigned to either three days of 88 hours of total sleep deprivation (N=15, 4 females) or 8 hours of sleep per night (N=9, 3 females), followed by a night of recovery sleep. Blood samples were collected hourly for a total of 120 hours (2880 samples total). In study 2, 18 participants (6 females) were randomly assigned to 8 h/night (N=8) or 4 h/night (N=10) for 12 days. Blood samples were collected every half hour for a 24-hour period on baseline and day 10 of sleep restriction (1728 samples total). Plasma renin activity, aldosterone levels, urine output, and sodium excretion will be assessed in order to investigate RAAS. Cystatin C, estimated glomerulus filtration rate (eGFR), and urinary albumin to creatinine ratio (ACR) will be measured as indicators of renal function. This will be the first study to investigate the renal function during severe, acute total sleep deprivation and prolonged, repeated sleep restriction.
|Program type||Career Development Award|
|Effective start/end date||04/01/2019 → 03/31/2022|