González-Albarrán O, Ruilope L M, Villa E, García Robles R
Department of Endocrinology, Hospital Ramón y Cajal, Madrid, Spain.
Diabetes Res Clin Pract. 1998 Apr;39 Suppl:S15-26. doi: 10.1016/s0168-8227(98)00018-7.
Almost two decades ago, the existence of a subset of essential hypertensive patients, who were sensitive (according to the increase in blood pressure levels) to the intake of a diet with a high salt content, was described. These patients are characterized by an increase in blood pressure and in body weight when switched from a low to a high sodium intake. The increase in body weight is due to the incapacity of the kidneys to excrete the whole intake of sodium until renal perfusion pressure (mean blood pressure) attains a level that is able to restore pressure-natriuresis relationship to values that enable the kidney to excrete the salt ingested or administered intravenously. Salt sensitivity does not seem to depend on the existence of an intrinsic renal defect to handle sodium, but on the existence of subtle abnormalities in the regulation of the sympathetic nervous system, the renin-angiotensin system or endothelial function. It is also relevant that organ damage secondary to arterial hypertension, has been shown in animal models and in hypertensive humans sensitive to a high salt intake to be significantly higher when compared with that of salt-resistant animals or humans. Interestingly, in humans, salt sensitivity has been shown to correlate with microalbuminuria, an important predictor of cardiovascular morbidity and mortality, which correlates with most of the cardiovascular risk factors commonly associated with arterial hypertension. One of these factors is insulin resistance, that usually accompanies high blood pressure in overweight and obese hypertensives. Insulin resistance and hyperinsulinism are present in a significant percentage of hypertensive patients developing cardiovascular symptoms or death. For these reasons, therapy of arterial hypertension must be directed, not only to facilitate the lowering of BP level, but also, to halt the mechanisms underlying the increase in BP, when salt intake is increased. Furthermore, therapy must preferably improve the diminished insulin sensitivity present in salt-sensitive subjects that contribute independently to increased cardiovascular risk.
大约二十年前，就已描述了一类原发性高血压患者的存在，这类患者（根据血压水平的升高情况）对高盐饮食的摄入敏感。这些患者的特点是，从低钠摄入转为高钠摄入时，血压和体重会增加。体重增加是由于肾脏无法排泄全部摄入的钠，直到肾灌注压（平均血压）达到能够使压力-利钠关系恢复到能让肾脏排泄摄入或静脉注射的盐分的水平。盐敏感性似乎并不取决于处理钠的内在肾脏缺陷的存在，而是取决于交感神经系统、肾素-血管紧张素系统或内皮功能调节中存在的细微异常。同样相关的是，在动物模型和对高盐摄入敏感的高血压患者中，与盐抵抗的动物或人类相比，动脉高血压继发的器官损害已被证明明显更高。有趣的是，在人类中，盐敏感性已被证明与微量白蛋白尿相关，微量白蛋白尿是心血管发病率和死亡率的重要预测指标，它与大多数通常与动脉高血压相关的心血管危险因素相关。这些因素之一是胰岛素抵抗，它通常伴随超重和肥胖高血压患者的高血压出现。胰岛素抵抗和高胰岛素血症在出现心血管症状或死亡的高血压患者中占相当大的比例。出于这些原因，动脉高血压的治疗不仅必须致力于促进血压水平的降低，而且还必须在盐摄入量增加时阻止血压升高的潜在机制。此外，治疗最好能改善盐敏感受试者中存在的胰岛素敏感性降低，这种降低独立地导致心血管风险增加。
