Region-specific changes in sympathetic nerve activity in angiotensin II-salt hypertension in the rat.
Region-specific changes in sympathetic nerve activity in angiotensin II-salt hypertension in the rat.
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DOI：
10.1113/expphysiol.2008.046326
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发表时间：
2010-01
影响因子：
2.7
通讯作者：
Fink GD
中科院分区：
文献类型：
--
作者：
Osborn JW;Fink GD
现在人们普遍认为，许多形式的实验性高血压和人类原发性高血压是由交感神经系统活动增加引起的。然而，交感神经活动（SNA）的区域特异性变化在高血压发病机制中的作用一直难以确定，因为还没有在有意识的动物中慢性测量SNA的方法。我们最近结合了间接、连续和慢性直接的区域特异性SNA评估，以表征服用高盐饮食（Ang II -盐高血压）的大鼠血管紧张素II （Ang II -盐高血压）引起的高血压。在高盐饮食的大鼠中，血管紧张素II增加全身去甲肾上腺素（NA）溢出和神经节阻滞的抑制反应，但在正常盐饮食的大鼠中没有。尽管有证据表明Ang ii -盐高血压大鼠的“全身SNA”增加，但该模型中肾脏SNA降低，肾去神经支配并未减弱动脉压的稳态水平。此外，在angii -盐高血压大鼠中，腰椎SNA（主要针对骨骼肌）和后肢NA外溢均未从对照水平改变。然而，在angii -盐高血压大鼠中观察到，手术切除内脏血管床的神经可以减弱/消除动脉压和总外周阻力的增加，以及血管电容的下降。我们假设，angii -盐高血压的“交感信号”的特征是内脏SNA增加，骨骼肌SNA没有变化，肾脏SNA降低，这种交感信号产生了独特的血流动力学变化，能够产生持续的高血压。
It is now well accepted that many forms of experimental hypertension and human essential hypertension are caused by increased activity of the sympathetic nervous system. However, the role of region-specific changes in sympathetic nerve activity (SNA) in the pathogenesis of hypertension has been difficult to determine because methods for chronic measurement of SNA in conscious animals have not been available. We have recently combined indirect, and continuous and chronic direct, assessment of region-specific SNA to characterize hypertension produced by administration of angiotensin II (Ang II) to rats consuming a high-salt diet (Ang II–salt hypertension). Angiotensin II increases whole-body noradrenaline (NA) spillover and depressor responses to ganglionic blockade in rats consuming a high-salt diet, but not in rats on a normal-salt diet. Despite this evidence for increased ‘whole-body SNA’ in Ang II–salt hypertensive rats, renal SNA is decreased in this model and renal denervation does not attenuate the steady-state level of arterial pressure. In addition, neither lumbar SNA, which largely targets skeletal muscle, nor hindlimb NA spillover is changed from control levels in Ang II–salt hypertensive rats. However, surgical denervation of the splanchnic vascular bed attenuates/abolishes the increase in arterial pressure and total peripheral resistance, as well as the decrease in vascular capacitance, observed in Ang II–salt hypertensive rats. We hypothesize that the ‘sympathetic signature’ of Ang II–salt hypertension is characterized by increased splanchnic SNA, no change in skeletal muscle SNA and decreased renal SNA, and this sympathetic signature creates unique haemodynamic changes capable of producing sustained hypertension.
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DOI：
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发表时间：
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影响因子：
2.8
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