Salt-sensitive hypertension--update on novel findings.
Salt-sensitive hypertension--update on novel findings.
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DOI：
10.1093/ndt/gfl757
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发表时间：
2007-04
期刊：
影响因子：
--
通讯作者：
B. Rodriguez-Iturbe;N. Vaziri
中科院分区：
文献类型：
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作者：
B. Rodriguez-Iturbe;N. Vaziri
高盐摄入量和脉搏硬化之间的联系早在4500年前就已经知道了[1]，但我们对肾脏在钠引起的血压升高中所起的核心作用的理解植根于盖顿和他的同事的研究[2]，他们假设，盐摄入后恢复钠平衡依赖于钠尿反应，这种反应是由短暂的血压上升驱动的。从本质上讲，血压升高是一种生理反应，旨在维持钠平衡和细胞外容量(ECV)在正常范围内。负责血压-尿钠关系的机制受损将使曲线“右移”，因此需要更高的血压水平来实现维持体内平衡所需的尿钠排泄的增加，从而将系统重新设置为更高的血压水平。钠负荷几乎一致地与血压正常和高血压患者的血压升高有关[3]。因此，盐敏感性的概念意味着对钠平衡变化的夸大反应。使用最广泛的盐敏性评估方法是Weinberger等人提出的方法。[3]，这是基于使用低钠饮食(10mMol/天)加口服速尿，注射2 L生理盐水后发现的血压与钠耗竭后发现的血压之间的差值。盐敏感性被定义为盐负荷和盐缺乏状态之间的差异10 mm Hg和耐盐性的差异，即5 mm Hg。使用这些标准，51%的高血压人群(73%的非裔美国人高血压患者)和26%的正常血压个体对盐敏感[3]。虽然重复性问题一直困扰着许多研究，但Weinberger和他的同事报告的后续研究表明，盐敏感状态是持续的，随着时间的推移可以重现，而且盐敏感的血压正常的人比耐盐的人更容易患高血压[4]。此外，盐敏感型高血压患者的心血管事件发生率高出3倍[5]。有趣的是，盐敏感性与死亡率的增加无关，与血压无关[6]。如后文所述，这种现象指向钠的不利直接作用。
The association between a high salt intake and hardened pulse was already known 4500 years ago [1], but our understanding of the central role played by the kidneys in the sodium-driven increase in blood pressure is rooted in the studies of Guyton and co-workers [2], who postulated that restoration of sodium balance after salt intake depends on a natriuretic response, driven by a transient rise in blood pressure. In essence, the blood pressure increment serves as a physiological response directed to maintain sodium balance and extracellular volume (ECV) within normal limits. Impairment of the mechanisms responsible for the pressure-natriuresis relationship will shift the curve ‘to the right’, so that higher blood pressure levels are needed to achieve the increments in urinary sodium excretion required to maintain homeostasis and the system is thereby reset at a higher blood pressure level. Sodium loading is almost uniformly associated with an increase in blood pressure in normotensive and hypertensive individuals [3]. Therefore, the notion of salt sensitivity implies an exaggerated response to changes in sodium balance. The most widely used method of assessing salt sensitivity is that proposed by Weinberger et al. [3], which is based on the difference between the blood pressure found after administration of 2 l of saline and the blood pressure found after sodium depletion, using a low Na diet (10mMol/day) plus oral furosemide. Salt sensitivity was defined as a difference of 10mmHg between salt-loaded and saltdepleted states and salt-resistance, a difference of 5mmHg. Using these criteria, salt sensitivity was found in 51% of the hypertensive population (73% of African-American hypertensive patients) and 26% of the normotensive individuals [3]. While the problem of reproducibility has plagued many studies, Weinberger and co-workers have reported follow-up studies showing that a salt-sensitive state is persistent and reproducible over time and that salt-sensitive normotensive individuals develop hypertension more frequently than their salt-resistant counterparts [4]. Furthermore, salt-sensitive hypertensive patients have a 3-fold higher incidence of cardiovascular events [5]. Interestingly, salt sensitivity is associated with increased mortality independent of blood pressure [6]. As described later, this phenomenon points to the adverse direct actions of sodium.