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

Abstract

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...

Objective sleep, a novel risk factor for alterations in kidney function: the CARDIA study

“…High levels of eGFR are an early predictor of diabetes and hypertension [25,26], associated with increasing levels of pre-diabetes and pre-hypertension in the general population [27], and are associated with higher incidence rates of coronary heart disease and mortality [5]. We hypothesize, based on extant studies, that poor or short sleep may increase sympathetic nervous system activity [28], blunt normal falls in blood pressure that occur during sleep [29,30], and impair metabolic regulation [28,31]. These changes, in turn, may then increase eGFR to abnormally high levels, hence increasing the risk for glomerular hypertension, renal injury, and the development of CKD and CVD risk factors.…”

Epworth Sleepiness Scale may be an indicator for blood pressure profile and prevalence of coronary artery disease and cerebrovascular disease in patients with obstructive sleep apnea

“…For EDS subjects, elevation in BP may come from heightened sympathetic drive, elevated catecholamines, and increased cortisol level [25], then the explanation for higher ratio of nighttime/daytime average BP may be the disproportional increasing of these factors, which is more at night than daytime. Nocturnal BP decline or "dipping" is an active, central, nervously governed process, which is important for BP regulation during daytime [35]. The lack of nocturnal BP fall (nondipping) is closely associated with target organ damage and worsened cardiovascular outcomes [36].…”

Sleep and cardiovascular regulation

“…However, in these normal sleepers the effect was due to HR and BP values during arousals elevating average values, rather than an increase in values during the brief sleep periods [13]. Blood pressure dipping has also been shown to be attenuated in normal sleepers when the level of SWS is reduced by "EEG guided acoustical arousals" [54]. However, whether this is due to reduced SWS, as argued by the authors, or to pulsative BP activation in association with "sub-cortical arousals" remains unclear.…”