HIGHLIGHTED TOPIC Mechanisms of Sympathetic Regulation in Cardiovascular
HIGHLIGHTED TOPIC Mechanisms of Sympathetic Regulation in Cardiovascular
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发表时间：
2012
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通讯作者：
A. Gabor;F. Leenen
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作者：
A. Gabor;F. Leenen
Gabor A, Leenen FH。高血压患者交感神经活动的中枢神经调节通路。中国生物医学工程学报（英文版），2012(3):444 - 444。2012年7月5日首次发表；doi: 10.1152 / japplphysiol.00553.2012。经典的神经递质，谷氨酸和GABA，介导快速（毫秒）的突触传递，并通过缓慢（秒到分钟）的信号传导过程调节其有效性。从终板到室旁核(PVN)/视上核和延髓吻侧腹侧侧（RVLM）的血管紧张素能通路被循环血管紧张素II型（Ang II）、脑脊液钠离子浓度（[Na]）以及可能的血浆醛固酮等刺激激活，主要通过减少GABA和增加谷氨酸释放导致交感神经兴奋。醛固酮-内源性瓦巴因（EO）通路是一种较慢的神经调节通路。醛固酮促进EO释放，后者通过增加PVN中Ang I受体（AT1R）和NADPH氧化酶亚基的表达，从而增加血管紧张素能通路的慢性活性。阻断该通路不影响初始交感兴奋和压力反应，但在很大程度上阻止对CSF [Na]或Ang II的慢性反应。这两种神经调节通路的招募允许中枢神经系统（CNS）以一种有效的方式快速引起和维持交感神经过度活跃。在许多高血压模型中，GABA释放减少，谷氨酸释放增加，AT1R激活增强（如PVN和RVLM）导致血压升高。在Dahl S大鼠和自发性高血压大鼠中，高盐激活中枢神经系统醛固酮- eo通路，通过特异性阻断从醛固酮合成酶到AT1R级联中的任何步骤，可以预防/逆转盐诱导的高血压。需要进一步的研究来加深我们对大脑中这些快速、缓慢和非常缓慢的中枢神经系统通路在高血压和其他与慢性交感神经过度活跃相关的疾病状态中如何以及在何处被激活和相互作用的理解。
Gabor A, Leenen FH. Central neuromodulatory pathways regulating sympathetic activity in hypertension. J Appl Physiol 113: 1294–1303, 2012. First published July 5, 2012; doi:10.1152/japplphysiol.00553.2012.—The classical neurotransmitters, glutamate and GABA, mediate fast (milliseconds) synaptic transmission and modulate its effectiveness through slow (seconds to minutes) signaling processes. Angiotensinergic pathways, from the lamina terminalis to the paraventricular nucleus (PVN)/supraoptic nucleus and rostral ventrolateral medulla (RVLM), are activated by stimuli such as circulating angiotensin type II (Ang II), cerebrospinal fluid (CSF) sodium ion concentration ([Na ]), and possibly plasma aldosterone, leading to sympathoexcitation, largely by decreasing GABA and increasing glutamate release. The aldosterone-endogenous ouabain (EO) pathway is a much slower neuromodulatory pathway. Aldosterone enhances EO release, and the latter increases chronic activity in angiotensinergic pathways by, e.g., increasing expression for Ang I receptor (AT1R) and NADPH oxidase subunits in the PVN. Blockade of this pathway does not affect the initial sympathoexcitatory and pressor responses but to a large extent, prevents chronic responses to CSF [Na ] or Ang II. Recruitment of these two neuromodulatory pathways allows the central nervous system (CNS) to shift gears to rapidly cause and sustain sympathetic hyperactivity in an efficient manner. Decreased GABA release, increased glutamate release, and enhanced AT1R activation in, e.g., the PVN and RVLM contribute to the elevated blood pressure in a number of hypertension models. In Dahl S rats and spontaneous hypertensive rats, high salt activates the CNS aldosterone-EO pathway, and the salt-induced hypertension can be prevented/reversed by specific CNS blockade of any of the steps in the cascade from aldosterone synthase to AT1R. Further studies are needed to advance our understanding of how and where in the brain these rapid, slow, and very slow CNS pathways are activated and interact in models of hypertension and other disease states associated with chronic sympathetic hyperactivity.