Malatino L S, Bellanuova I, Cataliotti A, Cuzzola F, Mallamaci F, Tripepi G, Parlongo S, Cutrupi S, Mangiafico R A, Ferri C, Galletti F, Glorioso N, Strazzullo P, Zoccali C
Clinical Medicine L. Condorelli Institute, University of Catania, Italy.
J Nephrol. 2000 May-Jun;13(3):178-84.
We investigated the influence of salt intake on urinary and plasma endothelin-1 (ET-1) in 55 patients who entered a two-week double-blind, randomised, crossover study comparing a 50 mMol/day salt intake and 150 mMol/day. Twenty-four-hour ET-1 excretion and plasma ET-1 were measured by RIA on pre-extracted samples.
In the whole cohort (n=55), changes in urinary ET-1 were related to salt excretion (r=0.28, P=0.04) and urinary volume (r=0.47, P=0.0001). In a multivariable model, changes in PRA, plasma aldosterone, blood pressure and heart rate did not add any predictive power to salt excretion with regard to urinary ET-1 variations. The relationship between urinary volume and urinary ET-1 was stronger than that of urinary sodium with ET-1 excretion because sodium was excluded from the multivariable model when urinary volume was introduced. Changes in urinary ET-1 were unrelated to mean blood pressure changes (P=0.66). Changes in plasma ET-1 were unaffected by changes in salt intake (P=0.58) but were strongly related to those in PRA (r= -0.45, P=0.01) and plasma aldosterone (r= -0.53, P=0.002).
The renal excretion of ET-1 is influenced by changes in salt intake and appears largely independent of the blood pressure response to salt. Changes in urinary volume which accompany variations in salt excretion play an important role in this response. Since urinary ET-1 reflects its renal synthesis, our data support the notion that renal ET-1 plays a role in the regulation of sodium balance in patients with mild hypertension.
我们对55名患者进行了一项为期两周的双盲、随机、交叉研究,比较每日50毫摩尔和150毫摩尔的盐摄入量,以研究盐摄入对尿中和血浆中内皮素-1(ET-1)的影响。通过放射免疫分析法(RIA)对预先提取的样本测量24小时ET-1排泄量和血浆ET-1水平。
在整个队列(n = 55)中,尿ET-1的变化与盐排泄量(r = 0.28,P = 0.04)和尿量(r = 0.47,P = 0.0001)相关。在多变量模型中,对于尿ET-1的变化,血浆肾素活性(PRA)、血浆醛固酮、血压和心率的变化并未增加任何对盐排泄的预测能力。尿量与尿ET-1之间的关系比尿钠与ET-1排泄之间的关系更强,因为当引入尿量时,钠被排除在多变量模型之外。尿ET-1的变化与平均血压变化无关(P = 0.66)。血浆ET-1的变化不受盐摄入量变化的影响(P = 0.58),但与PRA的变化密切相关(r = -0.45,P = 0.01)和血浆醛固酮的变化密切相关(r = -0.53,P = 0.002)。
ET-1的肾脏排泄受盐摄入量变化的影响,并且在很大程度上独立于对盐的血压反应。伴随盐排泄变化的尿量变化在这种反应中起重要作用。由于尿ET-1反映其肾脏合成,我们的数据支持肾脏ET-1在轻度高血压患者钠平衡调节中起作用的观点。