American journal of hypertension · 2015
Sympathetic Hyperactivity, Sleep Fragmentation, and Wake-Related Blood Pressure Surge During Late-Light Sleep in Spontaneously Hypertensive Rats.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Lai Chun-Ting, Chen Chun-Yu, Kuo Terry B J, Chern Chang-Ming, Yang Cheryl C H
Аннотация
BACKGROUND: Many cardiovascular disease events occur before morning awaking and are more severe in hypertensive patients. Sleep-related cardiovascular regulation has been suggested to play an important role in the pathogenesis. In this study, we explored whether such impairments are exaggerated during late sleep (before the active phase) in spontaneously hypertensive rats (SHRs).
METHODS: Polysomnographic recording was performed through wireless transmission in freely moving SHRs and Wistar-Kyoto rats (WKYs) over 24 hours. The SHRs were injected with saline and an α1-adrenergic antagonist (prazosin: 5 mg/kg) on 2 separate days. Cardiovascular and autonomic functions were assessed by cardiovascular variability and spontaneous baroreflex analysis.
RESULTS: Compared with the early-light period (Zeitgeber time (ZT) 0-6 hours), both the WKYs and SHRs during the late-light period (ZT 6-12 hours) showed sleep fragmentation, sympathovagal imbalance, and baroreflex impairment, which were exaggerated and more advanced in the SHRs. Like the morning blood pressure (BP) surge in humans, we found that there was a wake-related blood pressure surge (WBPS) during the late-light period in both groups of rats. The WBPS was also greater and occurred earlier in the SHRs, and was accompanied by a surge in vascular sympathetic index. Under α1-adrenergic antagonism, the late-light period-related sleep fragmentation and BP surge in the SHRs were partially reversed.
CONCLUSIONS: Our results reveal that sleep-related sympathetic overactivity, baroreflex sensitivity impairment, WBPS, and sleep fragmentation in SHRs deteriorates during the late-light period can be partially alleviated by treatment with an α1-adrenoceptor antagonist.
METHODS: Polysomnographic recording was performed through wireless transmission in freely moving SHRs and Wistar-Kyoto rats (WKYs) over 24 hours. The SHRs were injected with saline and an α1-adrenergic antagonist (prazosin: 5 mg/kg) on 2 separate days. Cardiovascular and autonomic functions were assessed by cardiovascular variability and spontaneous baroreflex analysis.
RESULTS: Compared with the early-light period (Zeitgeber time (ZT) 0-6 hours), both the WKYs and SHRs during the late-light period (ZT 6-12 hours) showed sleep fragmentation, sympathovagal imbalance, and baroreflex impairment, which were exaggerated and more advanced in the SHRs. Like the morning blood pressure (BP) surge in humans, we found that there was a wake-related blood pressure surge (WBPS) during the late-light period in both groups of rats. The WBPS was also greater and occurred earlier in the SHRs, and was accompanied by a surge in vascular sympathetic index. Under α1-adrenergic antagonism, the late-light period-related sleep fragmentation and BP surge in the SHRs were partially reversed.
CONCLUSIONS: Our results reveal that sleep-related sympathetic overactivity, baroreflex sensitivity impairment, WBPS, and sleep fragmentation in SHRs deteriorates during the late-light period can be partially alleviated by treatment with an α1-adrenoceptor antagonist.