Translation of salt retention to central activation of the sympathetic nervous system in hypertension
Translation of salt retention to central activation of the sympathetic nervous system in hypertension
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DOI：
10.1111/j.1440-1681.2005.04206.x
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发表时间：
2005-05-01
影响因子：
2.9
通讯作者：
Johnson, AK
中科院分区：
文献类型：
--
作者：
Brooks, VL;Haywood, JR;Johnson, AK
1.增加饮食中的盐会增加许多高血压患者的血压，产生盐敏感性高血压（SSH）。原因不明，但主要成分似乎是交感神经系统的激活。这篇简短的综述的目的是提出一个假说来解释如何增加饮食中的盐增加交感神经活动在SSH.2。有人提出，盐摄入量增加会导致盐潴留，并提高血浆氯化钠（NaCl）浓度，从而激活钠/β受体，触发交感神经兴奋。此外，我们认为，小的和往往无法检测到的增加渗透压可以驱动显着的交感神经兴奋，因为增益的渗透压和交感神经活性增加之间的关系增强。多种因素可能有助于这种促进作用，包括血管紧张素II或醛固酮水平的不适当升高，基因表达或突触可塑性的变化以及脑脊液中钠浓度的增加.未来的研究需要描绘脑部位和作用机制和渗透压和这些放大因子的相互作用，以引起持续的交感兴奋SSH。
1. Increased dietary salt increases blood pressure in many hypertensive individuals, producing salt-sensitive hypertension (SSH). The cause is unknown, but a major component appears to be activation of the sympathetic nervous system. The purpose of this short review is to present one hypothesis to explain how increased dietary salt increases sympathetic activity in SSH.2. It is proposed that increased salt intake causes salt retention and raises plasma sodium chloride (NaCl) concentrations, which activate sodium/osmoreceptors to trigger sympathoexcitation. Moreover, we suggest that small and often undetectable increases in osmolality can drive significant sympathoexcitation, because the gain of the relationship between osmolality and increased sympathetic activity is enhanced. Multiple factors may contribute to this facilitation, including inappropriately elevated levels of angiotensin II or aldosterone, changes in gene expression or synaptic plasticity and increased sodium concentrations in cerebrospinal fluid.3. Future studies are required to delineate the brain sites and mechanisms of action and interaction of osmolality and these amplification factors to elicit sustained sympathoexcitation in SSH.