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《2015年全国睡眠呼吸学术年会论文汇编》2015年
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The role of the NOX4-DerivedROS-Mediated RhoA/Rho KinasePathway in CIH induced hypertension

Wen Lu  Jing Kang  Ke Hu  Xiufang Zhou  Si Tang  Shuhui Yu  Yuanyuan Li  Lifang Xu  
【摘要】:Background Obstructivesleep apnea syndrome is a risk factor for resistant hypertension,which is associated with many cardiovascular diseases such as hypertension and linked to oxidative stress.CIH elicits systemic oxidative stress and sympathetic hyperactivity,which led to hypertension.Rho-kinases(ROCKs)is most accept as major effectors of the small GTPase RhoA,and have been extensively studied in the field of cardiovascular research.Upregulation of the RhoA/ROCK signalling cascade has been observed in different cardiovascular disorders like atherosclerosis,pulmonary hypertension and stroke.Nevertheless,the exact molecular mechanism of RhoA/ROCK in CIH remains unclear and needs to be further studied.Objectives To investigate the role of NOX4-ROS-RhoA/ROCK pathway in the chronic intermittent hypoxia induced hypertensive rats.Methods Male Sprague-dawley rats were exposed to chronic intermittent hypoxia(CIH)for21 days(8h/day,alternating cycles of hypoxia and normoxia,each lasting 90s,nadir FiO2:10%).We randomly assigned 70 male rats toa chronic intermittent hypoxia group(CIH),a saline-treated CIH group(CIH-S),a DMSO-treated CIH group(CIHDMSO),a apocynin-treated CIH group(CIH-apo),a N-acetyl cysteine-treated CIH group(CIH-NAC),a fasudil-treated CIH group(CIH-F),and a room air group(RA).The RA group rats were exposed to chronic intermittent normoxia stimulation,Other groups were exposed to chronic intermittent hypoxia stimulation.Blood pressure was monitored before the experiment and 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 When compared with room air conditions,CIH rats showed significant blood pressure elevations,oxidative stress level,RSNA and NE and AngⅡlevel after exposure to CIH.This response was attenuated aftertreating animals with apocynin,NAC and fasudil.Theexpression of RhoA/ROCK pathway and NADPH oxidase 4(NOX4)increased in CIH rats,too.Inhibition of NOX4 activitydecreased the RhoA/ROCK protein expression and oxidative stress.Conclusion We suggest that the CIH contribute to hypertension by NOX4-derived ROS-mediated RhoA/ROCKpathway,inhibition of whichmay ameliorate kidney injurysignificantly in rats exposed to CIH.
【分类号】:R766;R544.1

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