Hypothalamic paraventricular nucleus activation contributes to neurohumoral excitation in rats with heart failure.
Hypothalamic paraventricular nucleus activation contributes to neurohumoral excitation in rats with heart failure.
复制标题
下丘脑室旁核激活有助于心力衰竭大鼠的神经体液兴奋
DOI：
10.1186/2050-490x-2-2
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发表时间：
2014-12
影响因子：
2
通讯作者：
Zhu GQ
中科院分区：
文献类型：
--
作者：
Kang YM;Yang Q;Yu XJ;Qi J;Zhang Y;Li HB;Su Q;Zhu GQ
心力衰竭（HF）是一种严重的心血管疾病，其特征是交感神经活动过度。在本文中，我们回顾了这些有限的研究，特别强调检查室旁核（PVN）在HF的神经体液兴奋的作用。室旁核是重要的神经内分泌和自主神经前输出核团，是交感神经活动整合的重要中枢部位。越来越多的证据表明，许多神经体液过程参与了HF的病理生理过程，如肾素-血管紧张素系统（RAS）、促炎细胞因子（PIC）、神经递质和活性氧（ROS）。近年来的神经体液调节研究表明，血管紧张素Ⅱ 1型受体（AT 1-R）是HF大鼠室旁核细胞质核因子-κ B（NF-κB B）介导的重要产物，其表达沿着PICs和血管紧张素Ⅱ（ANG Ⅱ）的升高而上调。这些结果表明NF-κB介导了HF时PVN中RAS和PIC之间的相互作用。进一步的研究表明，室旁核内AT 1-R与NF-κB相互作用，通过调节神经递质参与氧化应激和交感神经兴奋，超氧化物激活室旁核内NF-κB参与神经体液兴奋。结论：心衰时的神经体液兴奋是基于RAS、PIC、ROS、NF-κB和室旁核神经递质的相互作用;室旁核NF-κB的激活调节了室旁核神经递质，参与了心衰大鼠交感神经兴奋的过程。
Heart failure (HF) is a serious cardiovascular disease and is characterized by exaggerated sympathetic activity. In this paper, we review these limited studies, with particular emphasis on examining the role of the paraventricular nucleus (PVN) in the neurohumoral excitation in HF. The PVN is an important neuroendocrine and preautonomic output nucleus, and is considered as the important central site for integration of sympathetic nerve activity. Accumulating evidences demonstrate that a number of neurohumoral processes are involved in the pathophysiology of HF, such as renin-angiotensin system (RAS), proinflammatory cytokines (PICs), neurotransmitters, and reactive oxygen species (ROS). Recent studies about neurohumoral regulation indicate that angiotensin II type1 receptor (AT1-R) is the important product mediated by cytoplasmic nuclear factor-kappa B (NF-κB) which is up-regulated along with elevated PICs and angiotensin II (ANG II) in the PVN of HF rats. These findings suggest that the NF-κB mediates the cross-talk between RAS and PICs in the PVN in HF. The further studies indicate that the interaction between AT1-R and NF-κB in the PVN contributes to oxidative stress and sympathoexcitation by modulating neurotransmitters in heart failure, and the superoxide activates NF-κB in the PVN and contributes to neurohumoral excitation. In conclusion, the neurohumoral excitation in HF is based on the interaction of RAS, PICs, ROS, NF-κB and neurotransmitters in the PVN; and the activated NF-κB in the PVN modulates the neurotransmitters and contributes to sympathoexcitation in rats with heart failure.