睡眠不足与高血压和心血管疾病的风险增加有关。新兴研究表明,压力反射敏感性(BRS)受损与睡眠剥夺引起的不良心血管影响有关。然而,潜在的机制仍然未知。因此,本研究旨在阐明肾素-血管紧张素系统异常在睡眠剥夺引起的BRS受损中的作用。
■将大鼠随机分为两组:正常睡眠(Ctrl)和慢性睡眠剥夺(CSD)组。大鼠被自动睡眠剥夺系统剥夺睡眠。血压,心率,BRS,评估大鼠NTS中c-Fos阳性细胞的数量和血管紧张素(Ang)II亚型1受体(AT1R)的表达。
■与Ctrl组相比,CSD组血压较高,心率,减少BRS。此外,与Ctrl组相比,CSD组NTS中c-Fos阳性细胞数和局部场电位增加。结果表明,与Ctrl组相比,CSD组大鼠NTS中AT1R的表达和AngII的含量以及AngII与Ang-(1-7)的比例增加。此外,NTS微量注射氯沙坦可显着改善睡眠剥夺引起的BRS受损。
■总而言之,这些数据表明,NTS中AT1R表达的升高介导了慢性睡眠剥夺引起的BRS降低。
UNASSIGNED: Sleep insufficiency has been linked to an increased risk of high blood pressure and cardiovascular diseases. Emerging studies have demonstrated that impaired baroreflex sensitivity (BRS) is involved in the adverse cardiovascular effects caused by sleep deprivation, however, the underlying mechanisms remain unknown. Therefore, the present study aims to clarify the role of abnormal renin-angiotensin system in the nucleus tractus solitarii (NTS) in impaired BRS induced by sleep deprivation.
UNASSIGNED: Rats were randomly divided into two groups: normal sleep (Ctrl) and chronic sleep deprivation (CSD) group. Rats were sleep deprived by an automated sleep deprivation system. The blood pressure, heart rate, BRS, the number of c-Fos positive cells and the expression of angiotensin (Ang) II subtype 1 receptors (
AT1R) in the NTS of rats were assessed.
UNASSIGNED: Compared to Ctrl group, CSD group exhibited a higher blood pressure, heart rate, and reduced BRS. Moreover, the number of c-Fos positive cells and local field potential in the NTS in CSD group were increased compared with the Ctrl group. It was shown that the expression of the
AT1R and the content of Ang II and the ratio of Ang II to Ang-(1-7) were increased in the NTS of rats in CSD group compared to Ctrl group. In addition, microinjection of losartan into the NTS significantly improved the impaired BRS caused by sleep deprivation.
UNASSIGNED: In conclusion, these data suggest that the elevated
AT1R expression in the NTS mediates the reduced BRS induced by chronic sleep deprivation.