Sleep And Blood Pressure: Rem Stage's Effect

Blood pressure is mostly affected by sleep. During non-rapid eye movement (NREM) sleep, there is a decrease in blood pressure and sympathetic tone and an increase in parasympathetic tone. During rapid eye movement (REM) sleep, blood pressure and sympathetic tone return to the levels observed during wakefulness.

In a study on rats, it was found that systolic and diastolic blood pressure during all sleep stages (NREM, REM) and while awake (quiet, active) were significantly lower in hypocretin neuron-ablated rats.

In another study, it was found that the rate of occurrence of arterial pressure surges during REM sleep was higher in spontaneously hypertensive rats than in Wistar-Kyoto normotensive controls and a group of spontaneously hypertensive rats in which hypertension was prevented by long-term enalapril treatment. However, the magnitude of the surges was similar across the three groups.

In summary, blood pressure does increase during REM sleep.

Blood pressure variability during sleep in snorers with or without apnea

Snorers with or without apnea experience different blood pressure variability during sleep. In non-rapid eye movement (non-REM) sleep, which makes up about 80% of total sleep, normal subjects experience a decrease in blood pressure and bradycardia. In contrast, sleep apnea is associated with large swings in nocturnal blood pressure.

In a study by Van Surell et al., researchers evaluated a computer-derived index of all-night blood pressure variability in normotensive snorers with or without sleep apnea. They found that the standard deviation of the distribution of systolic and diastolic pressure variations was higher in the apneic groups than in the non-apneic groups. This indicates that those with sleep apnea experience greater variability in blood pressure during sleep.

Another study by Planès et al. investigated the influence of daytime blood pressure levels and aging on short-term blood pressure variability during sleep in patients with obstructive sleep apnea syndrome (OSAS). They found that apnoea-related systolic and diastolic blood pressure elevations were significantly greater in hypertensive subjects than in normotensive subjects. Additionally, short-term blood pressure variability was not significantly increased in normotensive elderly patients.

These findings suggest that systemic hypertension is associated with greater blood pressure variability during sleep in individuals with sleep apnea. Furthermore, aging does not appear to have a significant impact on blood pressure variability in this population.

It is important to note that the studies mentioned above focused on short-term blood pressure variability during sleep. Long-term blood pressure variability and its relationship with sleep apnea warrants further investigation. Additionally, the impact of different treatments for sleep apnea, such as continuous positive airway pressure (CPAP) therapy, on blood pressure variability during sleep requires further research.

REM sleep and hypertension

Hypertension is a common cardiovascular disease that affects a large number of people worldwide. It is characterised by an abnormally high blood pressure, which can lead to severe health complications, such as heart attacks and strokes. Understanding the factors that influence blood pressure is crucial for preventing and managing this condition. One factor that has been implicated in blood pressure regulation is sleep, particularly the REM (rapid eye movement) sleep stage.

Blood Pressure and Sleep

During sleep, the body's physiological functions slow down, leading to a decrease in blood pressure. This reduction in blood pressure during sleep is known as "dipping". However, this decrease is not uniform across all sleep stages. Studies have shown that blood pressure and heart rate tend to increase during the transition from non-REM (non-rapid eye movement) sleep to REM sleep. This increase in blood pressure and heart rate during REM sleep may contribute to the higher incidence of heart attacks observed in the early morning hours.

REM Sleep and Blood Pressure Surges

Several studies have reported surges or increases in blood pressure during REM sleep. These surges are associated with a decrease in heart period and an increase in electroencephalographic theta frequency. The underlying cause of these blood pressure surges is thought to be related to central neural mechanisms and an increase in sympathetic activity.

Hypertension and REM Sleep

The relationship between hypertension and REM sleep has been investigated in both animal models and human patients. Spontaneously hypertensive rats (SHR), a model for human essential hypertension, exhibit an increased rate of occurrence of blood pressure surges during REM sleep compared to normotensive control groups. This suggests that hypertension may play a role in triggering these surges. However, the magnitude of the surges was similar between hypertensive and normotensive groups, indicating that hypertension does not directly influence the intensity of the surges.

Mechanisms and Implications

The mechanisms underlying the increased rate of blood pressure surges during REM sleep in hypertension are not fully understood. One hypothesis suggests that hypertension enhances the frequency of central autonomic commands to the cardiovascular system, leading to more frequent surges. Additionally, the instability in autonomic functions during REM sleep may contribute to abrupt changes in blood pressure.

The clinical implications of these findings are significant. The increased rate of blood pressure surges during REM sleep in hypertension may contribute to acute cardiovascular events, such as myocardial infarction and stroke. Therefore, understanding the interaction between hypertension and REM sleep is crucial for the prevention and management of cardiovascular complications associated with this condition.

In conclusion, REM sleep is associated with alterations in blood pressure regulation, which may have important implications for individuals with hypertension. Further research is needed to fully elucidate the mechanisms underlying the relationship between REM sleep and hypertension, as well as the potential impact on cardiovascular health.

References

• Van de Borne, P., Nguyen, H., Biston, P., Linkowski, P., & Degaute, J. P. (1994). Effects of wake and sleep stages on the 24-h autonomic control of blood pressure and heart rate in recumbent men.. American Journal of Physiology-Heart and Circulatory Physiology, 266(4), H548–H554.
• Somers, V. K., Dyken, M. E., Mark, A. L., & Abboud, F. M. (1993). Sympathetic-nerve activity during sleep in normal subjects. New England Journal of Medicine, 328(3), 303–307.
• Sei, H., & Morita, Y. (1996). Acceleration of EEG theta wave precedes the phasic surge of arterial pressure during REM sleep in the rat. NeuroReport, 7(13), 3059–3062.
• Berteotti, C., Franzini, C., Lenzi, P., Zoccoli, G., & Silvani, A. (2008). Surges of arterial pressure during REM sleep in spontaneously hypertensive rats. Sleep, 31(1), 111–117.

REM sleep and cardiovascular events

Sleep has been shown to influence the cardiovascular system, with a decrease in blood pressure occurring during sleep in a variety of species. This phenomenon is generally referred to as "dipping". The sleep-related decrease in blood pressure occurs in addition to the blood pressure changes induced by the circadian clock and changes in body posture that typically accompany sleeping behaviours. A loss of the normal reduction in blood pressure during sleep is a predictive measure for increased cardiovascular morbidity. Dipping is influenced by a change in the activity of the autonomic nervous system, with non-dippers experiencing an increase in sympathetic tone at sleep onset, as opposed to the normal reduction in sympathetic and increase in parasympathetic tone.

Sleep state transitions are accompanied by changes in the cardiovascular system. For example, when transitioning from non-rapid eye movement (NREM) sleep to REM sleep, blood pressure and heart rate increase and become less stable. These cardiovascular changes that occur during NREM to REM transitions may underlie the observation of increased prevalence of heart attacks in the early morning hours.

In a study on rats, it was found that hypocretin neuron-ablated rats had significantly lower systolic and diastolic blood pressure during all sleep stages (NREM, REM) and while awake (quiet, active).

In another study, spontaneously hypertensive rats (SHR) were compared with Wistar-Kyoto normotensive controls (WKY) and a group of SHR in which hypertension was prevented by long-term enalapril treatment (ena-SHR). SHR showed a significant increase in the rate of occurrence but a similar magnitude of the pressure surges during REM sleep, with respect to WKY and ena-SHR. The pressure surges were associated with a decrease in heart period and an increase in electroencephalographic theta frequency, which were significantly less pronounced in SHR than in either WKY or ena-SHR.

In a study on 32 obstructive sleep apnea patients, no differences were detected in obstructive respiratory event duration or degree of desaturation between REM and NREM sleep. Additionally, no difference in blood pressure (systolic and diastolic) was detected between REM and NREM sleep during obstructive events and post-obstructive event period.

In summary, while blood pressure does increase during REM sleep, it also increases during NREM sleep. Therefore, it is difficult to establish a direct link between REM sleep and cardiovascular events. However, the increase in blood pressure during REM sleep may be one of several factors that contribute to the increased incidence of acute cardiovascular events in the early morning hours.

REM sleep and sympathetic nerve activity

Sleep is involved in the regulation of the cardiovascular system, with specific changes occurring during REM sleep. During REM sleep, blood pressure and heart rate increase and become less stable. This is due to an increase in sympathetic nerve activity, which is intrinsic to the brain processes of this sleep state.

During REM sleep, the electroencephalogram (EEG) displays a prevalent theta rhythm, which accelerates before the surge peak. The electromyogram (EMG) indicates muscle atonia, which is interrupted by muscle twitches.

The sympathetic nervous system is responsible for the increase in blood pressure and heart rate during REM sleep. This system is activated by central neural mechanisms, which may be linked to changes in muscle tone.

The increase in sympathetic nerve activity during REM sleep may be linked to triggering acute cardiovascular events, such as myocardial infarction and ischemic stroke, which have a higher incidence in the early morning hours after awakening.

REM sleep and the baroreceptor-heart rate reflex

The baroreceptor-heart rate reflex is a mechanism that helps to maintain blood pressure at a constant level. It does this by lowering the heart rate when blood pressure is high and increasing it when blood pressure is low. This mechanism is particularly important when dealing with postural hypotension, which is when blood pressure decreases upon standing due to gravity.

During REM sleep, blood pressure and heart rate increase and become less stable. These changes may be linked to the increased prevalence of heart attacks in the early morning hours, as transitions to REM sleep are more frequent during this time.

The baroreceptor-heart rate reflex is mediated by both the parasympathetic and sympathetic branches of the autonomic nervous system. Baroreceptors are stretch receptors that respond to the stretching of blood vessels. They are most sensitive in the carotid sinuses and aortic arch and send signals to the medulla oblongata.

During sleep, core body temperature, systolic and diastolic blood pressure, and heart rate are all affected. In particular, systolic and diastolic blood pressure, and heart rate are lower during non-REM sleep compared to when awake.

In a study on rats, it was found that hypocretin neuron-ablated rats had significantly lower systolic and diastolic blood pressure during all sleep stages, including non-REM and REM sleep, as well as when awake. This suggests that hypocretins are important in regulating baseline blood pressure and may also modulate the effects of sleep on blood pressure.

In another study, it was found that the rate of occurrence of arterial pressure surges during REM sleep was higher in spontaneously hypertensive rats compared to normotensive controls. These surges were associated with a decrease in heart period and an increase in electroencephalographic theta frequency, which were less pronounced in the spontaneously hypertensive rats.

In summary, the baroreceptor-heart rate reflex is an important mechanism that helps to regulate blood pressure during REM sleep. Changes in blood pressure and heart rate during REM sleep may be linked to an increased risk of heart attacks in the early morning hours. Additionally, hypocretins and hypertension may play a role in modulating the effects of sleep on blood pressure.

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