Haddy F J, Pamnani M B
Department of Physiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799, USA.
J Am Coll Nutr. 1995 Oct;14(5):428-38. doi: 10.1080/07315724.1995.10718533.
Hypertension is the most common chronic disease in the United States and, untreated, results in disability or death due to stroke, heart failure or kidney failure. Fortunately the results of hypertension can be avoided to a large extent by proper treatment. One treatment which is effective in some cases is the restriction of dietary NaCl intake. This review considers the role of dietary NaCl in the genesis, therapy and prevention of hypertension. Most people can eat as much NaCl as they like; they have good kidneys which, within about 24 hours, excrete the NaCl as fast as it is taken in and nothing happens to blood pressure. A few, especially those with kidney disease, do not excrete it as fast as it is taken in and blood pressure rises. They are "salt sensitive". Once hypertension is established, the proportion who are "NaCl sensitive" is much higher. About 60% of people with hypertension respond to a high NaCl intake with a rise in pressure and to NaCl restriction with a fall in pressure and reduction in the need for antihypertensive medication. These are the same people that respond to diuretics with a fall in blood pressure. Many are black and elderly and have low plasma renin activity (low-renin hypertension) but some have normal or high plasma renin activity (normal or high-renin hypertension). Evidence suggests that very early they have a subtle kidney defect which causes them to excrete NaCl and water more slowly, e.g., even before they become hypertensive, black and elderly subjects excrete intravenously administered NaCl more slowly than white and young subjects. How does NaCl retention raise blood pressure? One possibility is that the NaCl retention causes water retention which releases a digitalis-like substance that increases the contractile activity of heart and blood vessels. Another is that the sodium itself penetrates the vascular smooth muscle cell, causing it to contract. "Salt sensitive" hypertension also responds to increased potassium and calcium intakes, perhaps in part because they increase NaCl urinary excretion.
高血压是美国最常见的慢性疾病，若不加以治疗，会因中风、心力衰竭或肾衰竭导致残疾或死亡。幸运的是，通过适当治疗，高血压的后果在很大程度上是可以避免的。在某些情况下有效的一种治疗方法是限制饮食中氯化钠的摄入量。本综述探讨饮食中氯化钠在高血压的发生、治疗和预防中的作用。大多数人可以随心所欲地摄入氯化钠；他们的肾脏功能良好，在大约24小时内，会将摄入的氯化钠尽快排出，血压不会发生变化。少数人，尤其是患有肾脏疾病的人，排出氯化钠的速度不如摄入的速度快，血压就会升高。他们是“盐敏感者”。一旦患上高血压，“对氯化钠敏感”的人群比例会高得多。约60%的高血压患者在摄入高量氯化钠时血压会升高，而限制氯化钠摄入时血压会下降，且对降压药物的需求也会减少。这些人对利尿剂也会有血压下降的反应。许多人是黑人和老年人，血浆肾素活性较低（低肾素性高血压），但也有一些人的血浆肾素活性正常或较高（正常或高肾素性高血压）。有证据表明，在很早的时候他们就存在一种细微的肾脏缺陷，导致他们排出氯化钠和水的速度更慢，例如，甚至在他们患高血压之前，黑人和老年受试者静脉注射氯化钠后排出的速度就比白人和年轻受试者慢。氯化钠潴留是如何升高血压的呢？一种可能性是氯化钠潴留导致水潴留，从而释放出一种类似洋地黄的物质，增加心脏和血管的收缩活动。另一种可能性是钠本身穿透血管平滑肌细胞，使其收缩。“盐敏感型”高血压对增加钾和钙的摄入量也有反应，这可能部分是因为它们增加了尿中氯化钠的排泄。
