Total Sleep Deprivation Elevates Blood Pressure Through Arterial Baroreflex Resetting: a Study with Microneurographic Technique

Ogawa, Yasuaki; Kanbayashi, Takashi; Saitō, Yasushi; Takahashi, Yūji; Kitajima, Tsuyoshi; Takahashi, Ken­ichi; Hishikawa, Yasuo; Shimizu, Tetsuo

doi:10.1093/sleep/26.8.986

Cited by 185 publications

(151 citation statements)

References 15 publications

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“…These effects, however, were restricted to the first half of total sleep time, and it is unlikely that this small effect sustained throughout the second half of the night. Previous studies consistently demonstrated that total 17,26 or partial 6,27 sleep deprivation resulted in increased blood pressure the next day, whereas the subjects in our study with less SWS had lower blood pressure levels.…”

Section: Discussionsupporting

confidence: 58%

“…2,9,15 Several studies suggested that nocturnal blood pressure dipping is caused by a shift of the baroreflex set point toward lower blood pressure levels. 9,14,17 However, the question remains unresolved regarding whether this is an active process or the mere consequence of physical inactivity and sleep-related deprivation from external stimuli.…”

Section: Discussionmentioning

confidence: 99%

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To Dip or Not to Dip

et al. 2007

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Abstract-That sleep is accompanied by a blood pressure decrease is well known; however, the underlying physiology deserves further investigation. The present study examines in healthy subjects 2 main questions: is this dipping actively evoked? and what are the consequences of nondipping for daytime blood pressure? Nocturnal blood pressure was extrinsically elevated in 12 sleeping subjects to mean daytime values by continuously infused phenylephrine. This nondipping significantly lowered morning blood pressure during rest and 3 hours after resuming physical activity compared with a control condition (isotonic saline). Neither muscle sympathetic nerve activity nor sensitivity of ␣-adrenoceptors was reduced. However, the set point for initiation of regulatory responses through the baroreflex was clearly shifted toward lower blood pressure levels. Our results support the hypothesis of an actively regulated central mechanism for blood pressure resetting and set point consolidation of the baroreflex during nighttime sleep. This is suggested by the fact that extrinsically induced nondipping induces sustained decrease in blood pressure during the following morning through an actively lowered baroreflex set point. (Hypertension.

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 99%

To Dip or Not to Dip

et al. 2007

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“…Lack of SWS could attenuate dipping, and therefore inhibit mechanisms of baroreflex-mediated blood pressure resetting. Both fragmentation of sleep due to repetitive arousals as well as sleep deprivation result in nocturnal sympathoexcitation leading to a nondipping profile and increased blood pressure even during daytime (12,16,36). The latter has repeatedly been shown for conditions of sleep-disordered breathing and was hypothesized to reflect a pathophysiologic adaptation to the increased nocturnal sympathetic activity (2,19).…”

mentioning

confidence: 97%

“…Baroreflex mechanisms are increasingly recognized to be involved in the medium-term regulation of blood pressure in addition to their role in buffering acute blood pressure changes (17,24). The proper resetting of the baroreflex threshold during NREM sleep is probably one key factor for the beneficial effects of sleep-related blood pressure dipping on cardiovascular health (15,16) and was found to exert stabilizing effects for blood pressure regulation during the daytime period (22). Sleep disturbances, in contrast, are linked to deficits in blood pressure regulation.…”

mentioning

confidence: 99%

Effects of selective slow-wave sleep deprivation on nocturnal blood pressure dipping and daytime blood pressure regulation

Sayk

Teckentrup

Becker

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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turnal blood pressure (BP) decline or "dipping" is an active, central, nervously governed process, which is important for BP regulation during daytime. It is, however, not known whether the sleep process itself or, more specifically, slow-wave sleep (SWS) is important for normal dipping. Therefore, in the present study, healthy subjects (6 females, 5 males) were selectively deprived of SWS by EEG-guided acoustic arousals. BP and heart rate (HR) were monitored during experimental nights and the following day. Additionally, nocturnal catecholamine excretion was determined, and morning baroreflex function was assessed by microneurographic measurements of muscle sympathetic nerve activity (MSNA) and heart rate variability (HRV). Data were compared with a crossover condition of undisturbed sleep. SWS was successfully deprived leading to significantly attenuated mean arterial BP dipping during the first half (P Ͻ 0.05), but not during the rapid-eye-movement-dominated second half of total sleep; however, dipping still evolved even in the absence of SWS. No differences were found for nighttime catecholamine excretion. Moreover, daytime resting and ambulatory BP and HR were not altered, and morning MSNA and HRV did not differ significantly, indicating that baroreflex-mediated sympathoneural BP regulation was not affected by the preceding SWS deprivation. We conclude that in healthy humans the magnitude of nocturnal BP dipping is significantly affected by sleep depth. Deprivation of SWS during one night does not modulate the morning threshold and sensitivity of the vascular and cardiac baroreflex and does not alter ambulatory BP during daytime.nondipping; baroreflex; muscle sympathetic nerve activity UNDISTURBED NOCTURNAL SLEEP is a prerequisite for health and well being. Particularly a proper nocturnal blood pressure decline commonly termed "dipping" is important for cardiovascular health. This process is not merely the consequence of physical inactivity but is actively governed by the central nervous system and mediated by an interplay between the autonomic nervous system and (neuro-)endocrine pathways, some of which are rather sleep dependent, while others are subject to circadian rhythms (1, 13, 34). Importantly, this sleep-associated blood pressure decline does not induce any sympathetic counterregulation, which is in contrast to the vigorous baroreflex activation to a blood pressure decrease of the same degree in awake subjects.The sleep-dependent modulation of blood pressure seems to result from the sleep stage-specific integration between cardiovascular reflexes and decreased central autonomic commands (7,25). In fact, sympathetic nervous traffic to the vasculature continuously decreases with the progressive deepening of nonrapid-eye-movement (NREM) sleep (11,27). Such decrease of vasoconstrictive sympathetic activity to the muscle vascular bed combined with the decline of blood pressure indicates a downward resetting of sympathovagal baroreflex setpoints being most relevant during slow-wave sleep (SWS) (7,25). Ba...

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“…Experimentelle Daten zeigen zudem, dass Schlafentzug und eine reduzierte nächtliche Schlafzeit mit Anstiegen des Blutdrucks [22] und der C-reaktiven Proteinkonzentrationen [23] …”

Section: Folgen Des Gestörten Schlafsunclassified