Data_Sheet_1_Sleep deprivation reduces the baroreflex sensitivity through elevated angiotensin (Ang) II subtype 1 receptor expression in the nucleus tractus solitarii.ZIP

IntroductionSleep 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.MethodsRats 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.ResultsCompared 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.DiscussionIn conclusion, these data suggest that the elevated AT1R expression in the NTS mediates the reduced BRS induced by chronic sleep deprivation.

睡眠不足与高血压及心血管疾病风险增加的联系已得到证实。新兴研究表明，受损的血压反射敏感性（BRS）参与睡眠剥夺引起的负面心血管效应，然而，其潜在机制尚不明确。因此，本研究旨在阐明异常的肾素-血管紧张素系统在孤束核（NTS）中在睡眠剥夺引起的受损BRS中所扮演的角色。

方法：将大鼠随机分为两组：正常睡眠组（Ctrl）和慢性睡眠剥夺组（CSD）。通过自动化睡眠剥夺系统对大鼠进行睡眠剥夺。评估了大鼠的血压、心率、BRS、c-Fos阳性细胞数量以及NTS中血管紧张素（Ang）II亚型1受体（AT1R）的表达。

结果：与Ctrl组相比，CSD组表现出更高的血压、心率和降低的BRS。此外，与Ctrl组相比，CSD组NTS中的c-Fos阳性细胞数量和局部电场电位增加。研究表明，与Ctrl组相比，CSD组大鼠NTS中的AT1R表达、Ang II含量以及Ang II与Ang-(1–7)的比值均增加。此外，向NTS微注射洛沙坦显著改善了睡眠剥夺引起的受损BRS。

讨论：综上所述，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。