Reactive oxygen species in the paraventricular nucleus mediate the cardiac sympathetic afferent reflex in chronic heart failure rats
Reactive oxygen species in the paraventricular nucleus mediate the cardiac sympathetic afferent reflex in chronic heart failure rats
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室旁核中的活性氧介导慢性心力衰竭大鼠的心脏交感传入反射
DOI：
10.1016/j.ejheart.2007.07.004
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发表时间：
2007-10-01
影响因子：
18.2
通讯作者：
Zhu, Guo-Qing
中科院分区：
文献类型：
--
作者：
Han, Ying;Shi, Zhen;Zhu, Guo-Qing
本研究的目的是确定室旁核（PVN）中的活性氧（ROS）是否介导慢性心力衰竭（CHF）大鼠的心交感传入反射（CSAR）和血管紧张素II诱导的CSAR增强。通过肾交感神经活动（RSNA）对心外膜应用缓激肽的反应来评价CSAR。在CHF和假手术大鼠中，PVN微量注射超氧阴离子清除剂tempol或tiron几乎消除了CSAR，但超氧化物歧化酶抑制剂DETC增强了CSAR。PVN预处理与tempol或tiron取消，而DETC增强，血管紧张素II诱导的CSAR增强。CHF大鼠室旁核超氧阴离子和丙二醛（MDA）水平升高，但AT受体拮抗剂氯沙坦可使其恢复正常。室旁核微量注射Tempol可降低超氧阴离子和MDA水平，而心外膜应用缓激肽或室旁核微量注射血管紧张素II则使超氧阴离子和MDA水平升高。CHF大鼠中的水平高于假手术大鼠。这些结果表明，在CHF和假手术大鼠中，室旁核中的ROS介导CSAR以及室旁核中的血管紧张素II对CSAR的影响。室旁核内活性氧的增加与CHF时CSAR的增强有关。(c)2007年欧洲心脏病学会。出版社：Elsevier B.V版权所有。
The aim of this study was to determine whether reactive oxygen species (ROS) in the paraventricular nucleus (PVN) mediate both the cardiac sympathetic afferent reflex (CSAR) and angiotensin II-induced CSAR enhancement in chronic heart failure (CHF) rats. CSAR was evaluated from the responses of renal sympathetic nerve activity (RSNA) to epicardial application of bradykinin. In both CHF and shamoperated rats, PVN microinjection of the superoxide anion scavengers tempol or tiron almost abolished the CSAR, but the superoxide dismutase inhibitor DETC potentiated the CSAR. PVN pretreatment with tempol or tiron abolished, whereas DETC augmented, the angiotensin II-induced CSAR enhancement. In CHF rats, superoxide anion and malondialdehyde (MDA) levels in the PVN were increased, but were normalized by the AT, receptor antagonist losartan. PVN microinjection of tempol decreased superoxide anion and MDA levels, but epicardial application of bradykinin or PVN microinjection of angiotensin II increased superoxide anion and MDA to higher. levels in CHF rats than in sham-operated rats. These results indicate that ROS in the PVN mediates the CSAR and the effect of angiotensin II in the PVN on the CSAR in both CHF and sham-operated rats. Increased ROS in the PVN are involved in the enhanced CSAR in CHF. (c) 2007 European Society of Cardiology. Published by Elsevier B.V All rights reserved.