Inhibition of reactive oxygen species in hypothalamic paraventricular nucleus attenuates the renin-angiotensin system and proinflammatory cytokines in hypertension
Inhibition of reactive oxygen species in hypothalamic paraventricular nucleus attenuates the renin-angiotensin system and proinflammatory cytokines in hypertension
复制标题
抑制下丘脑室旁核中的活性氧可减弱高血压中的肾素-血管紧张素系统和促炎细胞因子
DOI：
10.1016/j.taap.2014.02.002
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发表时间：
2014-04-15
影响因子：
3.8
通讯作者：
Kang, Yu-Ming
中科院分区：
文献类型：
--
作者：
Su, Qing;Qin, Da-Nian;Kang, Yu-Ming
目的：探讨下丘脑室旁核（PVN）活性氧（ROS）清除剂（tempol）是否能抑制血管紧张素II（ANG II）诱导的高血压大鼠的肾素-血管紧张素系统（RAS）和促炎细胞因子（PIC），降低血压和交感神经活性。雄性Sprague-Dawley大鼠静脉输注ANG II（10 ng/kg/min）或生理盐水（NS）4周。这些大鼠用氧自由基清除剂tempol（TEMP，20 μ g/h）或载体（人工脑脊液，aCSF）双侧PVN输注治疗4周。ANG II输注导致平均动脉压（MAP）和肾交感神经活动（RSNA）增加。与对照组相比，这些ANG II输注大鼠的室旁核中gp 91（phox）（NAD（P）H氧化酶的亚单位）、血管紧张素转换酶（ACE）和白细胞介素-1 β（IL-1 β）水平也较高。治疗与室旁核灌注的TEMP衰减gp 91（phox），ACE和IL-1 β的过度表达的室旁核内，并降低交感神经活性和MAP在ANG II-infined rats.Conclusion：这些研究结果表明，ANG II输注诱导升高PIC和氧化应激的室旁核，这有助于交感兴奋高血压。抑制下丘脑室旁核的活性氧减少血管紧张素II诱导的高血压中的肾素-血管紧张素系统、促炎细胞因子和氧化应激(C)2014 Elsevier Inc. All rights reserved.
Aims: To explore whether reactive oxygen species (ROS) scavenger (tempol) in the hypothalamic paraventricular nucleus (PVN) attenuates renin-angiotensin system (RAS) and proinflammatory cytokines (PICs), and decreases the blood pressure and sympathetic activity in angiotensin II (ANG II)-induced hypertension.Methods and results: Male Sprague-Dawley rats were infused intravenously with ANG II (10 ng/kg per min) or normal saline (NS) for 4 weeks. These rats were treated with bilateral PVN infusion of oxygen free radical scavenger tempol (TEMP, 20 mu g/h) or vehicle (artificial cerebrospinal fluid, aCSF) for 4 weeks. ANG II infusion resulted in increased mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). These ANG II-infused rats also had higher levels of gp91(phox) (a subunit of NAD(P)H oxidase), angiotensin-converting enzyme (ACE), and interleukin-1beta (IL-1 beta) in the PVN than the control animals. Treatment with PVN infusion of TEMP attenuated the overexpression of gp91(phox), ACE and IL-1 beta within the PVN, and decreased sympathetic activity and MAP in ANG II-infused rats.Conclusion: These findings suggest that ANG II infusion induces elevated PICs and oxidative stress in the PVN, which contribute to the sympathoexcitation in hypertension. Inhibition of reactive oxygen species in hypothalamic paraventricular nucleus attenuates the renin-angiotensin system, proinflammatory cytokines and oxidative stress in ANG II-induced hypertension. (C) 2014 Elsevier Inc. All rights reserved.