de Wardener Hugh E, He Feng J, MacGregor Graham A
Department of Clinical Chemistry, Imperial College, Charing Cross Hospital Campus, London, United Kingdom.
Kidney Int. 2004 Dec;66(6):2454-66. doi: 10.1111/j.1523-1755.2004.66018.x.
Dietary salt is the major cause of the rise in the blood pressure with age and the development of high blood pressure in populations. However, the mechanisms whereby salt intake raises the blood pressure are not clear. Existing concepts focus on the tendency for an increase in extracellular fluid volume (ECV), but an increased salt intake also induces a small rise in plasma sodium, which increases a transfer of fluid from the intracellular to the extracellular space, and stimulates the thirst center. Accordingly, the rise in plasma sodium is responsible for the tendency for an increase in ECV. Although the change in ECV may have a pressor effect, the associated rise in plasma sodium itself may also cause the blood pressure to rise. There is some evidence in patients with essential hypertension and the spontaneously hypertensive rat (SHR) that plasma sodium may be raised by 1 to 3 mmol/L. An experimental rise in sodium concentration greater than 5 mmol/L induces pressor effects on the brain and on the renin-angiotensin system. Such a rise can also induce changes in cultured vascular tissue similar to those that occur in the vessels of humans and animals on a high sodium diet, independent of the blood pressure. We suggest that a small increase in plasma sodium may be part of the mechanisms whereby dietary salt increases the blood pressure.
膳食盐是随着年龄增长血压升高以及人群中高血压发生的主要原因。然而，盐摄入导致血压升高的机制尚不清楚。现有观点集中在细胞外液量（ECV）增加的趋势上，但盐摄入量增加也会导致血浆钠略有升高，这会促使液体从细胞内转移到细胞外空间，并刺激口渴中枢。因此，血浆钠的升高是ECV增加趋势的原因。虽然ECV的变化可能具有升压作用，但血浆钠的相关升高本身也可能导致血压升高。在原发性高血压患者和自发性高血压大鼠（SHR）中有一些证据表明，血浆钠可能会升高1至3 mmol/L。钠浓度实验性升高超过5 mmol/L会对大脑和肾素-血管紧张素系统产生升压作用。这种升高还可诱导培养的血管组织发生变化，类似于高钠饮食的人和动物血管中发生的变化，且与血压无关。我们认为，血浆钠的小幅升高可能是膳食盐升高血压机制的一部分。
