Neuron：高盐饮食增加高血压风险又添新证据

  近日，来自麦吉尔大学的研究人员发现，盐分的过度摄入或会“重编程”大脑，从而干扰大脑的一系列天然安全机制，这些机制可以帮助机体抑制动脉血压上升，相关研究刊登于国际制Neuron上。

  目前科学家们已经熟知盐分和高血压之间的关联，但是却并不清楚高水平盐分的摄入增加血压的分子机制，文章中，研究者通过对大鼠大脑的研究发现，在饮食中摄入大量的盐或可引发关键大脑回路的改变。

  研究者Bourque表示，我们发现如果大鼠在一段时间内饮食中的盐分摄入过高则会引发关键神经元发生生化改变，而这些特殊的神经元会将加压素释放到循环系统中；这种改变往往会涉及一种名为脑源性神经营养因子（BDNF）的神经营养性分子，而且会抑制其它细胞的特殊神经元的功能。

  研究结果表明，高盐分摄入可以通过机体的动脉压检测回路来抑制加压素神经元，而当大量盐分被消化一段时间后，这种天然安全机制的失活也将促进血压升高。研究人员表示，本文研究或可帮助理解盐分摄入和高血压之间的关联，未来还需要更多的研究来发现更多新型的靶点来开发潜在疾病干预策略。（转化医学网360zhyx.com）
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转化医学网推荐的原文阅读：

High Salt Intake Increases Blood Pressure via BDNF-Mediated Downregulation of KCC2 and Impaired Baroreflex Inhibition of Vasopressin Neurons
Neuron doi:10.1016/j.neuron.2014.12.048
Katrina Y. Choe, Su Y. Han, Perrine Gaub, Brent Shell, Daniel L. Voisin, Blayne A. Knapp, Philip A. Barker, Colin H. Brown, J. Thomas Cunningham, Charles W. Bourquecorrespondenceemail
The mechanisms by which dietary salt promotes hypertension are unknown. Previous work established that plasma [Na+] and osmolality rise in proportion with salt intake and thus promote release of vasopressin (VP) from the neurohypophysis. Although high levels of circulating VP can increase blood pressure, this effect is normally prevented by a potent GABAergic inhibition of VP neurons by aortic baroreceptors. Here we show that chronic high salt intake impairs baroreceptor inhibition of rat VP neurons through a brain-derived neurotrophic factor (BDNF)-dependent activation of TrkB receptors and downregulation of KCC2 expression, which prevents inhibitory GABAergic signaling. We show that high salt intake increases the spontaneous firing rate of VP neurons in vivo and that circulating VP contributes significantly to the elevation of arterial pressure under these conditions. These results provide the first demonstration that dietary salt can affect blood pressure through neurotrophin-induced plasticity in a central homeostatic circuit.