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Sleep Disorders: Sleep Disorders III |

The Role of the NOX4-derived ROS-mediated RhoA/Rho Kinase Pathway in Rat Hypertension Induced by CIH FREE TO VIEW

Ke Hu, MD; Wen Lu; Jing Kang; Si Tang; Xiufang Zhou
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Renmin Hospital of Wuhan University, Wuhan, China


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;149(4_S):A581. doi:10.1016/j.chest.2016.02.606
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SESSION TITLE: Sleep Disorders III

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: To investigate the role of the NADPH oxidase 4 (NOX4)-ROS-RhoA/ROCK pathway in CIH-induced hypertensive rats.

METHODS: Male Sprague-Dawley rats were exposed to CIH for 21 days (intermittent hypoxia for 60 s with 21% O2 and for 30 s with 10% O2 cyclically repeated for 8 h/day). We randomly assigned 56 male rats to a normoxia group (RA), an untreated CIH group (uCIH), and CIH groups treated with saline (CIH-S), dimethyl sulfoxide (CIH-D), apocynin (CIH-A), N-acetyl cysteine (CIH-N), and fasudil (CIH-F). Rats in the RA group were exposed to room-air stimulation, whereas rats in the other groups were exposed to CIH stimulation. BP was monitored at the start and of each week. After the experiment, renal sympathetic nerve activity (RSNA) was recorded, and serum and renal tissues were used for molecular biological and biochemical detection.

RESULTS: Compared with the BP of RA rats, that of uCIH rats (without any drug intervention) started to increase two weeks after the experiment, subsequently stabilizing at a high level until the end of the third week. CIH caused increased sensitivity to both RSNA and oxidative stress. This response was attenuated after treating the rats with apocynin and NAC. Inhibition of NOX4 activity and ROS reduced RhoA/ROCK expression. Fasudil intervention reduced BP even though the rats were exposed to intermittent hypoxia, but did not affect RSNA.

CONCLUSIONS: Hypertension can be induced by CIH in SD rats. Disequilibrium of the NOX4-derived ROS-mediated RhoA/ROCK pathway may be the underlying mechanism.

CLINICAL IMPLICATIONS: CIH-induced hypertension is mediated by increased oxidative stress through the activation of NOX4 and its downstream RhoA/ROCK pathway in vivo. Elevation in RSNA also precedes hypertension. Inhibition of this pathway may have clinical significance in the treatment of OSA patients.

DISCLOSURE: The following authors have nothing to disclose: Ke Hu, Wen Lu, Jing Kang, Si Tang, Xiufang Zhou

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