Braam Branko, Huang Xiaohua, Cupples William A, Hamza Shereen M
Department of Medicine, University of Alberta, Edmonton, AB, Canada.
Department of Physiology, University of Alberta, Edmonton, AB, Canada.
Curr Hypertens Rep. 2017 Jun;19(6):49. doi: 10.1007/s11906-017-0744-z.
Fierce debate has developed whether low-sodium intake, like high-sodium intake, could be associated with adverse outcome. The debate originates in earlier epidemiological studies associating high-sodium intake with high blood pressure and more recent studies demonstrating a higher cardiovascular event rate with both low- and high-sodium intake. This brings into question whether we entirely understand the consequences of high- and (very) low-sodium intake for the systemic hemodynamics, the kidney function, the vascular wall, the immune system, and the brain. Evolutionarily, sodium retention mechanisms in the context of low dietary sodium provided a survival advantage and are highly conserved, exemplified by the renin-angiotensin system. What is the potential for this sodium-retaining mechanism to cause harm? In this paper, we will consider current views on how a sodium load is handled, visiting aspects including the effect of sodium on the vessel wall, the sympathetic nervous system, the brain renin-angiotensin system, the skin as "third compartment" coupling to vascular endothelial growth factor C, and the kidneys. From these perspectives, several mechanisms can be envisioned whereby a low-sodium diet could potentially cause harm, including the renin-angiotensin system and the sympathetic nervous system. Altogether, the uncertainties preclude a unifying model or practical clinical guidance regarding the effects of a low-sodium diet for an individual. There is a very strong need for fundamental and translational studies to enhance the understanding of the potential adverse consequences of low-salt intake as an initial step to facilitate better clinical guidance.
低钠摄入是否会像高钠摄入一样与不良后果相关，引发了激烈的争论。这场争论源于早期将高钠摄入与高血压联系起来的流行病学研究，以及最近显示低钠和高钠摄入都会导致更高心血管事件发生率的研究。这就引发了一个问题，即我们是否完全理解高钠和（极低）钠摄入对全身血流动力学、肾功能、血管壁、免疫系统和大脑的影响。从进化角度来看，在低膳食钠情况下的钠潴留机制提供了生存优势且高度保守，肾素 - 血管紧张素系统就是例证。这种钠潴留机制造成危害的可能性有多大？在本文中，我们将探讨当前关于钠负荷如何处理的观点，涉及钠对血管壁、交感神经系统、脑肾素 - 血管紧张素系统、作为与血管内皮生长因子C耦合的“第三间隙”的皮肤以及肾脏的影响等方面。从这些角度可以设想，低钠饮食可能通过多种机制造成危害，包括肾素 - 血管紧张素系统和交感神经系统。总之，这些不确定性使得无法形成一个关于低钠饮食对个体影响的统一模型或实用临床指南。迫切需要进行基础研究和转化研究，以加深对低盐摄入潜在不良后果的理解，作为促进更好临床指导的第一步。
