Bing R F, Thurston H, Swales J D
Lancet. 1979 Jul 21;2(8134):121-3. doi: 10.1016/s0140-6736(79)90004-7.
24 h urinary sodium excretion was used to monitor salt intake in 36 patients with essential hypertension to determine whether limitation of the antihypertensive action of thiazide diuretics could be explained by increased salt appetitie stimulated by salt depletion. Sodium excretion in these patients was similar before treatment to that observed in normotensive controls, and no change was observed during 2 years' treatment with bendrofluazide. However, plasma-renin rose progressively over the 2 years even in 5 of 8 patients whose renin was not stimulated initially by diuretics. Thus, there is no evidence that a voluntary increase in salt intake limits the efficacy of diuretic treatment; on the other hand, progressive stimulation of the renin-angiotensin system may be an important limiting factor to the antihypertensive action of diuretics. If so, the antihypertensive effect of dietary salt restriction may be similarly limited.
采用24小时尿钠排泄量来监测36例原发性高血压患者的盐摄入量，以确定噻嗪类利尿剂降压作用受限是否可由盐耗竭刺激的盐食欲增加来解释。这些患者治疗前的钠排泄量与血压正常的对照组相似，在使用苄氟噻嗪治疗的2年期间未观察到变化。然而，即使在最初利尿剂未刺激肾素分泌的8例患者中的5例中，血浆肾素在2年中也逐渐升高。因此，没有证据表明盐摄入量的自主增加会限制利尿剂治疗的疗效；另一方面，肾素-血管紧张素系统的逐渐激活可能是利尿剂降压作用的一个重要限制因素。如果是这样，限制饮食中盐的摄入所产生的降压作用可能同样受到限制。
