INTRODUCTION HYPOTHESIS RESULTS CONCLUSIONS  Growing evidence suggests that insufficient sleep is a risk factor for hypertension. 1,2  Nocturnal BP significantly.

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INTRODUCTION HYPOTHESIS RESULTS CONCLUSIONS  Growing evidence suggests that insufficient sleep is a risk factor for hypertension. 1,2  Nocturnal BP significantly decreases during sleep, especially during slow-wave sleep (SWS) 3 and surges in response to morning awakening. 3 Exaggerated post-rising morning BP surge 5 and failure of nocturnal BP dipping are strong predictors of adverse cardiovascular outcomes after adjusting for other covariates. 4  The purpose of the present study was to examine the influences of repeated bouts of sleep restriction (SR), with insufficient recovery sleep intervening (Fig 1), on 24h continuous BP/heart rate (HR) fluctuations (e.g. daytime, nighttime, nocturnal dipping and morning surge).  Our underlying hypothesis is that sleep plays a critical role in CNS autonomic homeostasis.  We predicted that SR would attenuate nocturnal BP and HR dipping in a dose-dependent manner and lead to an exaggerated BP and HR morning surge, such that later cycles (Fig 1) would show greatest impairment of function. METHODS  Repeated SR induced significant sustained attenuation of nocturnal BP dipping (Figure 2, 3), while HR dipping was increased across the cycles (Figure 5).  Repeated SR increased morning surge of BP and HR progressively through 4 cycles (Figure 6). Blunted Nocturnal Blood Pressure Dipping and Exaggerated Morning Blood Pressure Surge in Response to a Novel Repetitive Sleep Restriction Challenge Huan Yang 1, Monika Haack 1, Mackenzie S Lamanna 1 and Janet M. Mullington 1 1 Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, REFERENCES 1. Gangwisch JE. A review of evidence for the link between sleep duration and hypertension. Am J Hypertension 2014;27: Mullington JM, Haack M, Toth M, Serrador JM, and Meier-Ewert HK. Cardiovascular, inflammatory, and metabolic consequences of sleep deprivation. Progress in Cardiovascular Diseases 2009;51: Javaheri S and Redline S. Sleep, slow-wave sleep, and blood pressure. Curr Hypertens Rep 2012;14: Hansen TW, Li Y, Boggia J, Thijs L and Staessen JA, et al. Predictive role of the nighttime blood pressure. Hypertension 2011;57: Li Y, Thijs L, Hansen TW, Kikuya M and Staessen JA, et al. Prognostic value of the morning blood pressure surge in 5645 subjects from 8 populations. Hypertension 2010;55: Special thanks to the nurses and staffs in the Clinical Research Center (CRC) at BIDMC. Research Support: NHLBI (R01HL to Dr. Janet M. Mullington). And Harvard Catalyst CTSC NIH UL1 TR Table 1. Participants Characteristics. Values are mean ± SE; SR, sleep restriction; SC, sleep control; SAP/DAP/MAP, systolic/diastolic/mean arterial pressure, units, mmHg; HR, heart rate, unit, beats/min. VariableControl (n=22)Sleep Restriction (n=21)P Value Women/men11/1111/10- Age, years31± BMI, kg/m224± SAP, mmHg112±3107± DAP, mmHg67±165± MAP, mmHg83±280± HR, beats/min77±374± Habitual sleep, h7.8± Figure 2. Averaged hourly beat-to-beat mean arterial pressure in sleep restriction (SR) group. *P<0.05 compare to BL. Blue bar at the bottom indicates 8h sleep, whereas red bar represents 4h sleep. Figure 4. Averaged hourly beat-to-beat heart rate (HR) in sleep restriction (SR) group. *P<0.05 compare to BL. Blue and read bars indicate 8h vs 4h sleep. Figure 5. Nocturnal heart rate dipping in sleep restriction and control groups. *P<0.05 compare to baseline (BL); Ϯ P<0.05 compare to control. Figure 6. Morning mean arterial pressure (MAP; left) and heart rate (right) surges in sleep restriction and control groups. *P<0.05 compare to baseline (BL); Ϯ P<0.05 compare to control. Figure 3. Nocturnal mean arterial pressure dipping in sleep restriction and control groups. *P<0.05 compare to baseline (BL); Ϯ P<0.05 compare to control. Program#: 957.8