A common neuronal mechanism of hypertension and sleep disturbances in spontaneously hypertensive rats: Role of orexinergic neurons
A common neuronal mechanism of hypertension and sleep disturbances in spontaneously hypertensive rats: Role of orexinergic neurons
复制标题
自发性高血压大鼠高血压和睡眠障碍的常见神经机制：食欲能神经元的作用
DOI：
10.1016/j.pnpbp.2020.109902
复制
发表时间：
2020-06-08
影响因子：
5.6
通讯作者：
Zhang, Yong-He
中科院分区：
文献类型：
--
作者：
Cui, Su-Ying;Huang, Yuan-Li;Zhang, Yong-He
流行病学研究表明，睡眠障碍与高血压的发生有关。本研究调查了自发性高血压大鼠(SHR)在高血压发展过程中睡眠模式的动态变化，以及这些共病的神经机制，重点关注食欲素能系统。使用无创血压尾带测量大鼠的血压。通过脑电和肌电记录监测睡眠情况。免疫组织化学方法检测穹隆周围核内食欲素能神经元的密度和活性。下丘脑外侧区微量注射hcrt2-SAP(400或800 ng)损毁食欲素能神经元。与Wistar-京都大鼠相比，SHR表现出不同的睡眠障碍模式。在SHR中，大鼠活动期过度睡眠的动态变化与高血压的发展不同步，而静止期的过度觉醒和入睡困难与高血压的发展是同步的。此外，SHR穹隆周围核中食欲素能神经元的密度和活性明显高于同龄Wistar-京都大鼠。下丘脑外侧区食欲素能神经元的减少部分改善了SHR的高血压发展，预防了SHR入睡困难。这些结果表明，尽管睡眠障碍和高血压之间的关系非常复杂，但共同的机制可能是SHR这些共病的基础。食欲素系统的过度活跃可能是这样一种常见的机制。
Epidemiologic studies have shown that sleep disorders are associated with the development of hypertension. The present study investigated dynamic changes in sleep patterns during the development of hypertension across the lifespan in spontaneously hypertensive rats (SHRs) and the neural mechanism that underlies these comorbidities, with a focus on the orexinergic system. Blood pressure in rats was measured using a noninvasive blood pressure tail cuff. Sleep was monitored by electroencephalographic and electromyographic recordings. Immunohistochemistry was used to detect the density and activity of orexinergic neurons in the perifornical nucleus. Hcrt2-SAP (400 or 800 ng) was microinjected in the lateral hypothalamus to lesion orexinergic neurons. Compared with Wistar-Kyoto rats, SHRs exhibited various patterns of sleep disturbances. In SHRs, dynamic changes in hypersomnia in the rats' active phase was not synchronized with the development of hypertension, but hyperarousal in the inactive phase and difficulties in falling asleep were observed concurrently with the development of hypertension. Furthermore, the density and activity of orexinergic neurons in the perifornical nucleus were significantly higher in SHRs than in age-matched Wistar-Kyoto rats. The reduction of orexinergic neurons in the lateral hypothalamus partially ameliorated the development of hypertension and prevented difficulties in falling asleep in SHRs. These results indicate that although the correlation between sleep disturbances and hypertension is very complex, common mechanisms may underlie these comorbidities in SHRs. Overactivity of the orexin system may be one such common mechanism.