Laragh J H, Sealey J E, Bühler F R, Vaughan E D, Brunner H R, Gavras H, Baer L
Am J Med. 1975 Jan;58(1):4-13. doi: 10.1016/0002-9343(75)90527-6.
Information defining the renin-angiotension-aldosterone axis as a control system concurrently regulating salt balance and blood pressure has been applied to reexamine the role of renin in experimental and clinical forms of renovascular and renal hypertension, and thence to develop criteria for differentiating these entities. Experimentally, there are two models of renovascular hypertension; one is characterized by excess renin with reduced sodium (vasoconstrictor form) and the other by excess sodium with reduced renin (volume form). But with sodium depletion, the volume form converts to a vasoconstrictor form illustrating how the two factors coordinate to maintain blood pressure. In man, renovascular and renal hypertensions appear to be sustained by the same two mechanisms. Studies in man show that, in the absence of unilateral disease, the supine renal venous renin level in each kidney is consistently 24 percent higher than the peripheral level. Because of this constant relationship, the peripheral renin level is a measure of the renal secretion rate. Our studies indicate the curable unilateral renovascular hypertension is, in fact, renin-dependent vasoconstrictor hypertension. Three criteria, derived from four renin measurements, identify this situation: (1) Hypersecretion of renin is reflected by a high peripheral level when indexed against sodium excretion. (2) Lateralization of renin secretion with contralateral suppression rules out occult bilateral disease. It is indicated by V-A equal 0 from the uninvolved kidney. (3) (V-A)/A greater than 48 per cent from the ipsilateral kidney supports unilateralization. With data derived from patients with essential hypertension as a reference, the degree to which (V-A)/A is greater than 0.48 can be used to estimate the degree of renal ischemia, using Fick's principle. Corroborative evidence to support these three criteria can be developed from the blood pressure response to angiotensin blocking drugs or to antirenin therapy with propranolol. Clinical analysis validates these criteria to identify curable hypertension from unilateral renovascular or parenchymal disease. In patients with either occult or overt bilateral renal disease, the volume factor often predominates and is expressed by some suppression of plasma renin levels. Continued
将肾素 - 血管紧张素 - 醛固酮轴定义为同时调节盐平衡和血压的控制系统的相关信息，已被用于重新审视肾素在肾血管性高血压和肾性高血压的实验及临床形式中的作用，从而制定区分这些病症的标准。在实验中，有两种肾血管性高血压模型；一种以肾素过多伴钠减少为特征（血管收缩型），另一种以钠过多伴肾素减少为特征（容量型）。但当钠耗竭时，容量型会转变为血管收缩型，这说明了这两个因素如何协同维持血压。在人类中，肾血管性高血压和肾性高血压似乎由相同的两种机制维持。对人类的研究表明，在不存在单侧疾病的情况下，每个肾脏的仰卧位肾静脉肾素水平始终比外周水平高24%。由于这种恒定关系，外周肾素水平可作为肾分泌率的一个指标。我们的研究表明，可治愈的单侧肾血管性高血压实际上是肾素依赖性血管收缩型高血压。从四项肾素测量得出的三个标准可识别这种情况：（1）当以钠排泄为指标时，外周水平高反映肾素分泌过多。（2）肾素分泌的侧化伴对侧抑制可排除隐匿性双侧疾病。未受累肾脏的V - A等于0可表明这一点。（3）同侧肾脏的（V - A）/A大于48%支持单侧性。以原发性高血压患者的数据为参考，根据菲克原理，（V - A）/A大于0.48的程度可用于估计肾缺血的程度。支持这三个标准的确凿证据可从血压对血管紧张素阻断药物或普萘洛尔抗肾素治疗的反应中得出。临床分析证实了这些标准可用于从单侧肾血管性或实质性疾病中识别可治愈的高血压。在隐匿性或显性双侧肾脏疾病患者中，容量因素往往占主导，表现为血浆肾素水平有所抑制。续
