Abstract P017: Increased Sodium Excretion And Urinary Output During Acute Human Sleep Deprivation

Abstract

Introduction: Insufficient sleep contributes to an increased risk (e.g. ~60%) of hypertension. While BP is influenced by renal regulation of sodium and water, the underlying mechanism involved the modulation of renin-angiotensin-aldosterone-system (RAAS) by sleep deprivation is unknown. This project investigated the RAAS regulation of water and salt balance (e.g. urine output, sodium excretion) during prolonged sleep deprivation in humans. Methods: Twenty-six subjects (35±1 yrs; 9 women) completed a highly controlled 7-day in hospital study. They were randomly assigned to an 88-h total sleep deprivation (TSD; N=17) condition or an 8-h/night sleep control (SC; N=9) condition. Twenty-four-hour urinary output was collected from baseline (Day 2) to recovery (Day 7). Water and sodium intake were controlled and data were collected. The 24-h sodium excretion value (mmol) was calculated by multiplying the concentrations of sodium in the urine by the urinary volume. Frequent blood samples were collected throughout the experimental period in this study. Results: There was a significant interaction effect of TSD on sodium excretion and urinary output (condition x day, p<0.05). Both TSD and SC groups showed continuous increases in sodium excretion during experimental period compared to baseline (p<0.05). The increases in TSD were significantly higher compared to SC (condition x day, p<0.05). In addition, there was a dose dependent effect of TSD on sodium excretion (i.e. p<0.05 for 48-h TSD compared to 24-h TSD). Diet and fluid intake were controlled and there was no interaction effect for TSD on 24-h water intake or oral sodium intake (condition x day, p>0.05). Urinary output significantly increased from baseline, to 24-h and 72-h (p<0.05) during TSD, but remained at baseline levels throughout days in SC group. Preliminary plasma renin activity analyses (assays ongoing) showed a decreasing statistical trend during TSD compared to baseline (p=0.058). Conclusion: Prolonged TSD significantly increases sodium excretion and urinary output from the body compared to control group, despite similar water and sodium intake levels between two groups. In addition, the increases of sodium excretion are also dose dependent during TSD.