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No elevated plasma catecholamine levels during sleep in newly diagnosed, untreated hypertensives.

Rasch B, Dodt C, Sayk F, Mölle M, Born J - PLoS ONE (2011)

Bottom Line: We sampled blood at a fast rate (1/10 min) and monitored blood pressure and heart rate continuously.We show that plasma NE and E levels did not differ between hypertensives and normotensive during sleep as well as before and after sleep.Blood pressure was higher in hypertensives, reaching the largest group difference in the morning after sleep.

View Article: PubMed Central - PubMed

Affiliation: Department of Neuroendocrinology, University of Lübeck, Lübeck, Germany. Rasch@kfg.uni-luebeck.de

ABSTRACT
The sympatho-adrenergic system is highly involved in regulating sleep, wake and arousal states, and abnormalities in this system are regarded as a key factor in the development and progression of arterial hypertension. While hypertension is associated with a hyperadrenergic state during wakefulness, the effect of hypertension on plasma-catecholamine levels during sleep is not yet known. Twelve young participants with newly diagnosed, untreated hypertension and twelve healthy controls slept for 7 hours in the sleep laboratory. Before and after sleep, subjects rested in a supine position for 3-h periods of wakefulness. We sampled blood at a fast rate (1/10 min) and monitored blood pressure and heart rate continuously. We show that plasma NE and E levels did not differ between hypertensives and normotensive during sleep as well as before and after sleep. Blood pressure was higher in hypertensives, reaching the largest group difference in the morning after sleep. Unlike in the normotensives, in the hypertensive participants the morning rise in blood pressure did not correlate with the rise in catecholamine levels at awakening. Our results suggest that hypertension in its early stages is not associated with a strong hyperadrenergic state during sleep. In showing a diminished control of blood pressure through sympatho-adrenergic signals in hypertensive participants, our data point towards a possible involvement of dysfunctional sleep-related blood pressure regulation in the development of hypertension.

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Heart rate, blood pressure and plasma catecholamines in 12 normotensive (thin line) and 12 hypertensive men (thick line) during nocturnal sleep and a period of wakefulness of 3.5 hours before and after the sleep phase.Heart rate and blood pressure were measured continuously, blood for the determination of catecholamines was drawn every 10 min during the sleep period. Profiles were averaged across individuals and time locked to sleep onset and awakening in the morning, respectively. Bars indicate significant differences (P<0.05) for post hoc comparison when ANOVA indicated overall significance for the factor condition (night-time vs. daytime sleep).
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pone-0021292-g002: Heart rate, blood pressure and plasma catecholamines in 12 normotensive (thin line) and 12 hypertensive men (thick line) during nocturnal sleep and a period of wakefulness of 3.5 hours before and after the sleep phase.Heart rate and blood pressure were measured continuously, blood for the determination of catecholamines was drawn every 10 min during the sleep period. Profiles were averaged across individuals and time locked to sleep onset and awakening in the morning, respectively. Bars indicate significant differences (P<0.05) for post hoc comparison when ANOVA indicated overall significance for the factor condition (night-time vs. daytime sleep).

Mentions: In contrast to the notion of an sympatho-adrenergic over activation in hypertension, we did not observe any significant group differences between average levels of NE or E during the pre-wake, sleep and post-wake periods, respectively (main effect group NE: F(1,22)  = 1.1, E: F(1,22)  = 0.0; both P>0.30). Generally, the concentrations of NE and E were significantly lower during sleep than during wakefulness (main effect sleep/wake NE: F(2,44)  = 23.5, p<0.001; E: F(2,44)  = 6.1, P<0.01; Figure 1), and, these general effects were similarly observed in hypertensives as well as normotensives as indicated by non-significant interaction terms (interaction group * sleep/wake for NE and E concentrations: both P>0.28). In an analysis of all succeeding time points of blood sampling during the periods of interest (Figure 2), NE concentrations were revealed to be even significantly lower in the hypertensives as compared to the normotensive controls during most of the pre-sleep wake interval. During sleep, hypertensives still exibited lower NE levels on a descriptive level, although these differences were non-significant (see Figure 2). During sleep, plasma catecholamine concentrations distinctly varied depending on the sleep stage, with linearly decreasing values as sleep deepens, reaching minimal levels during REM sleep (main effect of stage for NE and E concentrations, respectively: F(4,88)  = 4.95; P<0.01 and F(4,88)  = 7.36; P<0.001). The effect of sleep stages on NE and E concentration did not differ between hypertensives vs. normotensives (interaction group * sleep stage: F(4,88)  = 2.12; P>0.10 and F(4,88)  = 0.45; P>0.50).


No elevated plasma catecholamine levels during sleep in newly diagnosed, untreated hypertensives.

Rasch B, Dodt C, Sayk F, Mölle M, Born J - PLoS ONE (2011)

Heart rate, blood pressure and plasma catecholamines in 12 normotensive (thin line) and 12 hypertensive men (thick line) during nocturnal sleep and a period of wakefulness of 3.5 hours before and after the sleep phase.Heart rate and blood pressure were measured continuously, blood for the determination of catecholamines was drawn every 10 min during the sleep period. Profiles were averaged across individuals and time locked to sleep onset and awakening in the morning, respectively. Bars indicate significant differences (P<0.05) for post hoc comparison when ANOVA indicated overall significance for the factor condition (night-time vs. daytime sleep).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3117886&req=5

pone-0021292-g002: Heart rate, blood pressure and plasma catecholamines in 12 normotensive (thin line) and 12 hypertensive men (thick line) during nocturnal sleep and a period of wakefulness of 3.5 hours before and after the sleep phase.Heart rate and blood pressure were measured continuously, blood for the determination of catecholamines was drawn every 10 min during the sleep period. Profiles were averaged across individuals and time locked to sleep onset and awakening in the morning, respectively. Bars indicate significant differences (P<0.05) for post hoc comparison when ANOVA indicated overall significance for the factor condition (night-time vs. daytime sleep).
Mentions: In contrast to the notion of an sympatho-adrenergic over activation in hypertension, we did not observe any significant group differences between average levels of NE or E during the pre-wake, sleep and post-wake periods, respectively (main effect group NE: F(1,22)  = 1.1, E: F(1,22)  = 0.0; both P>0.30). Generally, the concentrations of NE and E were significantly lower during sleep than during wakefulness (main effect sleep/wake NE: F(2,44)  = 23.5, p<0.001; E: F(2,44)  = 6.1, P<0.01; Figure 1), and, these general effects were similarly observed in hypertensives as well as normotensives as indicated by non-significant interaction terms (interaction group * sleep/wake for NE and E concentrations: both P>0.28). In an analysis of all succeeding time points of blood sampling during the periods of interest (Figure 2), NE concentrations were revealed to be even significantly lower in the hypertensives as compared to the normotensive controls during most of the pre-sleep wake interval. During sleep, hypertensives still exibited lower NE levels on a descriptive level, although these differences were non-significant (see Figure 2). During sleep, plasma catecholamine concentrations distinctly varied depending on the sleep stage, with linearly decreasing values as sleep deepens, reaching minimal levels during REM sleep (main effect of stage for NE and E concentrations, respectively: F(4,88)  = 4.95; P<0.01 and F(4,88)  = 7.36; P<0.001). The effect of sleep stages on NE and E concentration did not differ between hypertensives vs. normotensives (interaction group * sleep stage: F(4,88)  = 2.12; P>0.10 and F(4,88)  = 0.45; P>0.50).

Bottom Line: We sampled blood at a fast rate (1/10 min) and monitored blood pressure and heart rate continuously.We show that plasma NE and E levels did not differ between hypertensives and normotensive during sleep as well as before and after sleep.Blood pressure was higher in hypertensives, reaching the largest group difference in the morning after sleep.

View Article: PubMed Central - PubMed

Affiliation: Department of Neuroendocrinology, University of Lübeck, Lübeck, Germany. Rasch@kfg.uni-luebeck.de

ABSTRACT
The sympatho-adrenergic system is highly involved in regulating sleep, wake and arousal states, and abnormalities in this system are regarded as a key factor in the development and progression of arterial hypertension. While hypertension is associated with a hyperadrenergic state during wakefulness, the effect of hypertension on plasma-catecholamine levels during sleep is not yet known. Twelve young participants with newly diagnosed, untreated hypertension and twelve healthy controls slept for 7 hours in the sleep laboratory. Before and after sleep, subjects rested in a supine position for 3-h periods of wakefulness. We sampled blood at a fast rate (1/10 min) and monitored blood pressure and heart rate continuously. We show that plasma NE and E levels did not differ between hypertensives and normotensive during sleep as well as before and after sleep. Blood pressure was higher in hypertensives, reaching the largest group difference in the morning after sleep. Unlike in the normotensives, in the hypertensive participants the morning rise in blood pressure did not correlate with the rise in catecholamine levels at awakening. Our results suggest that hypertension in its early stages is not associated with a strong hyperadrenergic state during sleep. In showing a diminished control of blood pressure through sympatho-adrenergic signals in hypertensive participants, our data point towards a possible involvement of dysfunctional sleep-related blood pressure regulation in the development of hypertension.

Show MeSH
Related in: MedlinePlus