Sleep disturbance among spontaneously hypertensive rats is mediated by an α1-adrenergic mechanism

Terry B J Kuo, Chun Yu Chen, Chun Ting Lai, Tsai Yu Chuan, Wen Yi Wu, Shih Chih Tsai, Cheryl C H Yang

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Background Inadequate sleep may aggravate hypertension, but the pathophysiology of sleep disturbance in hypertension remains unknown. Among spontaneously hypertensive rats (SHR), sleep disturbance co-occurred with sympathetic hyperactivity; therefore, we hypothesized that the sleep disturbance can be alleviated by antagonizing the adrenergic overdrive. MethodsPolysomnographic recording was performed in SHR by telemetry. The animals were first injected with saline, and 2 days later with a hypotensive agent. Cardiac and vascular sympathetic activity were assessed using the normalized low-frequency power (LF%) of heart rate variability and the low-frequency power of arterial pressure variability (BLF), respectively.ResultsA comparison was made between the saline and hypotensive drug treatments. During quiet sleep (QS), the α1-blocker prazosin induced a significant decrease in BLF, but had no effect on LF%. The total time and bout duration of QS were lengthened and QS interruption was reduced (P 0.05 for all). When both α1-and α2-adrenoceptors were blocked by phentolamine, both BLF and LF% were lower (P 0.05 for both), but no modification to sleep structure could be observed. To antagonize Β-adrenergic activity, atenolol and propranolol were injected. The LF% after either antagonist treatment was significantly decreased; however, sleep structure was not significantly changed. The QS-promoting effect of prazosin is specific to SHR, because prazosin is ineffective when administered to Wistar-Kyoto rats.Conclusionsα1-adrenergic antagonism may reverse, at least partially, the poor sleep quality of SHR, suggesting a vicious cycle can be established between adrenergic overdrive and sleep disturbance.

Original languageEnglish
Pages (from-to)1110-1117
Number of pages8
JournalAmerican Journal of Hypertension
Volume25
Issue number10
DOIs
Publication statusPublished - Oct 2012
Externally publishedYes

Fingerprint

Inbred SHR Rats
Adrenergic Agents
Sleep
Prazosin
Hypertension
Telemetry
Atenolol
Inbred WKY Rats
Phentolamine
Propranolol
Adrenergic Receptors
Blood Vessels
Arterial Pressure
Heart Rate
Power (Psychology)

Keywords

  • β-adrenergic antagonist
  • â-adrenergic antagonist
  • blood pressure
  • hypertension
  • sleep
  • spontaneously hypertensive rat
  • sympathetic activity
  • telemetry

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Sleep disturbance among spontaneously hypertensive rats is mediated by an α1-adrenergic mechanism. / Kuo, Terry B J; Chen, Chun Yu; Lai, Chun Ting; Chuan, Tsai Yu; Wu, Wen Yi; Tsai, Shih Chih; Yang, Cheryl C H.

In: American Journal of Hypertension, Vol. 25, No. 10, 10.2012, p. 1110-1117.

Research output: Contribution to journalArticle

Kuo, Terry B J ; Chen, Chun Yu ; Lai, Chun Ting ; Chuan, Tsai Yu ; Wu, Wen Yi ; Tsai, Shih Chih ; Yang, Cheryl C H. / Sleep disturbance among spontaneously hypertensive rats is mediated by an α1-adrenergic mechanism. In: American Journal of Hypertension. 2012 ; Vol. 25, No. 10. pp. 1110-1117.
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abstract = "Background Inadequate sleep may aggravate hypertension, but the pathophysiology of sleep disturbance in hypertension remains unknown. Among spontaneously hypertensive rats (SHR), sleep disturbance co-occurred with sympathetic hyperactivity; therefore, we hypothesized that the sleep disturbance can be alleviated by antagonizing the adrenergic overdrive. MethodsPolysomnographic recording was performed in SHR by telemetry. The animals were first injected with saline, and 2 days later with a hypotensive agent. Cardiac and vascular sympathetic activity were assessed using the normalized low-frequency power (LF{\%}) of heart rate variability and the low-frequency power of arterial pressure variability (BLF), respectively.ResultsA comparison was made between the saline and hypotensive drug treatments. During quiet sleep (QS), the α1-blocker prazosin induced a significant decrease in BLF, but had no effect on LF{\%}. The total time and bout duration of QS were lengthened and QS interruption was reduced (P 0.05 for all). When both α1-and α2-adrenoceptors were blocked by phentolamine, both BLF and LF{\%} were lower (P 0.05 for both), but no modification to sleep structure could be observed. To antagonize Β-adrenergic activity, atenolol and propranolol were injected. The LF{\%} after either antagonist treatment was significantly decreased; however, sleep structure was not significantly changed. The QS-promoting effect of prazosin is specific to SHR, because prazosin is ineffective when administered to Wistar-Kyoto rats.Conclusionsα1-adrenergic antagonism may reverse, at least partially, the poor sleep quality of SHR, suggesting a vicious cycle can be established between adrenergic overdrive and sleep disturbance.",
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T1 - Sleep disturbance among spontaneously hypertensive rats is mediated by an α1-adrenergic mechanism

AU - Kuo, Terry B J

AU - Chen, Chun Yu

AU - Lai, Chun Ting

AU - Chuan, Tsai Yu

AU - Wu, Wen Yi

AU - Tsai, Shih Chih

AU - Yang, Cheryl C H

PY - 2012/10

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N2 - Background Inadequate sleep may aggravate hypertension, but the pathophysiology of sleep disturbance in hypertension remains unknown. Among spontaneously hypertensive rats (SHR), sleep disturbance co-occurred with sympathetic hyperactivity; therefore, we hypothesized that the sleep disturbance can be alleviated by antagonizing the adrenergic overdrive. MethodsPolysomnographic recording was performed in SHR by telemetry. The animals were first injected with saline, and 2 days later with a hypotensive agent. Cardiac and vascular sympathetic activity were assessed using the normalized low-frequency power (LF%) of heart rate variability and the low-frequency power of arterial pressure variability (BLF), respectively.ResultsA comparison was made between the saline and hypotensive drug treatments. During quiet sleep (QS), the α1-blocker prazosin induced a significant decrease in BLF, but had no effect on LF%. The total time and bout duration of QS were lengthened and QS interruption was reduced (P 0.05 for all). When both α1-and α2-adrenoceptors were blocked by phentolamine, both BLF and LF% were lower (P 0.05 for both), but no modification to sleep structure could be observed. To antagonize Β-adrenergic activity, atenolol and propranolol were injected. The LF% after either antagonist treatment was significantly decreased; however, sleep structure was not significantly changed. The QS-promoting effect of prazosin is specific to SHR, because prazosin is ineffective when administered to Wistar-Kyoto rats.Conclusionsα1-adrenergic antagonism may reverse, at least partially, the poor sleep quality of SHR, suggesting a vicious cycle can be established between adrenergic overdrive and sleep disturbance.

AB - Background Inadequate sleep may aggravate hypertension, but the pathophysiology of sleep disturbance in hypertension remains unknown. Among spontaneously hypertensive rats (SHR), sleep disturbance co-occurred with sympathetic hyperactivity; therefore, we hypothesized that the sleep disturbance can be alleviated by antagonizing the adrenergic overdrive. MethodsPolysomnographic recording was performed in SHR by telemetry. The animals were first injected with saline, and 2 days later with a hypotensive agent. Cardiac and vascular sympathetic activity were assessed using the normalized low-frequency power (LF%) of heart rate variability and the low-frequency power of arterial pressure variability (BLF), respectively.ResultsA comparison was made between the saline and hypotensive drug treatments. During quiet sleep (QS), the α1-blocker prazosin induced a significant decrease in BLF, but had no effect on LF%. The total time and bout duration of QS were lengthened and QS interruption was reduced (P 0.05 for all). When both α1-and α2-adrenoceptors were blocked by phentolamine, both BLF and LF% were lower (P 0.05 for both), but no modification to sleep structure could be observed. To antagonize Β-adrenergic activity, atenolol and propranolol were injected. The LF% after either antagonist treatment was significantly decreased; however, sleep structure was not significantly changed. The QS-promoting effect of prazosin is specific to SHR, because prazosin is ineffective when administered to Wistar-Kyoto rats.Conclusionsα1-adrenergic antagonism may reverse, at least partially, the poor sleep quality of SHR, suggesting a vicious cycle can be established between adrenergic overdrive and sleep disturbance.

KW - β-adrenergic antagonist

KW - â-adrenergic antagonist

KW - blood pressure

KW - hypertension

KW - sleep

KW - spontaneously hypertensive rat

KW - sympathetic activity

KW - telemetry

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