Role of paraventricular nucleus in mediating sympathetic outflow in heart failure.
Role of paraventricular nucleus in mediating sympathetic outflow in heart failure.
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DOI：
10.1023/a:1009850224802
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发表时间：
2000-03-01
影响因子：
4.6
通讯作者：
Patel, K P
中科院分区：
文献类型：
--
作者：
Patel, K P
在心力衰竭时，许多神经体液过程被激活，包括血浆去甲肾上腺素浓度的增加。很少有研究探讨中枢神经系统在心力衰竭(HF)时交感神经流出的激活中所起的作用。在这篇文章中，我回顾了这些有限的研究，特别强调了室旁核(PVN)在心力衰竭中常见的夸大交感神经流出中的作用。结论是，心力衰竭与大脑特定区域的变化有关，PVN内神经元激活的变化可能与心力衰竭状态下观察到的加压素产生、血容量调节和交感神经兴奋的异常有关。此外，室旁核内通过GABA机制参与调节交感神经流出的神经元一氧化氮可能缺乏抑制交感神经流出的能力，从而导致通常在心力衰竭中观察到的交感神经过度流出。
A number of neurohumoral processes are activated in heart failure, including an increase in the plasma concentration of norepinephrine. Few studies have been performed to examine the role of the central nervous system in the activation of sympathetic outflow during heart failure (HF). In this paper I review these limited studies, with particular emphasis on examining the role of the paraventricular nucleus (PVN) in the exaggerated sympathetic outflow commonly observed in heart failure. The conclusion is that heart failure is associated with changes in specific areas in the brain and that alterations in the activation of neurons in the PVN are likely related to abnormalities in vasopressin production, blood volume regulation, and sympathoexcitation observed in the heart failure state. Furthermore, neuronal nitric oxide within the PVN that is involved in mediating sympathetic outflow via a GABA mechanism from the PVN may be deficient in inhibiting overall sympathetic outflow leading to the exaggerated sympathetic outflow commonly observed in heart failure.