Hypothalamic paraventricular nucleus activation contributes to neurohumoral excitation in rats with heart failure.

IF 2 Regenerative Medicine Research Pub Date : 2014-01-08 eCollection Date: 2014-12-01 DOI:10.1186/2050-490X-2-2
Yu-Ming Kang, Qing Yang, Xiao-Jing Yu, Jie Qi, Yan Zhang, Hong-Bao Li, Qing Su, Guo-Qing Zhu
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引用次数: 22

Abstract

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.

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心衰大鼠下丘脑室旁核激活参与神经体液兴奋。
心衰(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,我们回顾这些有限的研究,特别强调检查室旁核(PVN)在心衰的神经体液兴奋中的作用。PVN是重要的神经内分泌和自主神经前输出核,被认为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心衰的病理生理,如肾素-血管紧张素系统(RAS)、促炎细胞因子(PICs)、神经递质和活性氧(ROS)。近年来关于神经体液调节的研究表明,血管紧张素II型1受体(AT1-R)是胞质核因子κB (NF-κB)介导的重要产物,在HF大鼠PVN中随着PICs和血管紧张素II (ANG II)的升高而上调。上述结果提示,NF-κB介导心衰患者PVN中RAS和PICs之间的串扰。进一步研究表明,心衰时PVN内AT1-R与NF-κB的相互作用通过调节神经递质导致氧化应激和交感神经兴奋,超氧化物激活PVN内NF-κB,促进神经体液兴奋。综上所述,HF的神经体液兴奋是基于RAS、PICs、ROS、NF-κB和PVN内神经递质的相互作用;心衰大鼠PVN活化的NF-κB调节神经递质,参与交感神经兴奋。
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Regenerative Medicine Research
Regenerative Medicine Research MEDICINE, RESEARCH & EXPERIMENTAL-
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