Neurogenic and sympathoexcitatory actions of NaCl in hypertension.
Neurogenic and sympathoexcitatory actions of NaCl in hypertension.
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DOI：
10.1007/s11906-013-0385-9
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发表时间：
2013-12
影响因子：
5.6
通讯作者：
Browning, Kirsteen N.
中科院分区：
文献类型：
--
作者：
Stocker, Sean D.;Monahan, Kevin D.;Browning, Kirsteen N.
关键词：
膳食盐摄入过多是盐敏感性高血压发病的一个主要因素。强有力的证据表明，盐敏感性高血压归因于肾功能障碍、血管异常和交感神经系统激活。事实上，在许多盐敏感模型中，交感神经横断或神经传递中断可以降低许多盐敏感模型的动脉血压（ABP）。本文的目的是讨论支持血浆或脑脊液高钠血症作为交感神经兴奋和 ABP 升高的关键介质的最新证据。使用时间控制采样的实验和临床研究都证明，高盐饮食会增加血浆和脑脊液的钠浓度。据测试，钠浓度的急性和慢性升高会激活动物和人类的交感神经系统。进一步了解中枢神经系统如何检测血浆或脑脊液钠浓度的变化可能会导致盐敏感性高血压的新治疗策略。
Excess dietary salt intake is a major contributing factor to the pathogenesis of salt-sensitive hypertension. Strong evidence suggests that salt-sensitive hypertension is attributed to renal dysfunction, vascular abnormalities, and activation of the sympathetic nervous system. Indeed, sympathetic nerve transections or interruption of neurotransmission in various brain centers lowers arterial blood pressure (ABP) in many salt-sensitive models. The purpose of this article is to discuss recent evidence that supports a role of plasma or cerebrospinal fluid hypernatremia as a key mediator of sympathoexcitation and elevated ABP. Both experimental and clinical studies using time-controlled sampling have documented that a diet high in salt increases plasma and cerebrospinal fluid sodium concentration. To the extent it has been tested, acute and chronic elevations in sodium concentration activates the sympathetic nervous system in animals and humans. A further understanding of how the central nervous system detects changes in plasma or cerebrospinal fluid sodium concentration may lead to new therapeutic treatment strategies in salt-sensitive hypertension.
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