Benmansour M, Caillens H, Ardaillou R
Nephrologie. 1980;1(3):109-12.
The effect of inhibition of angiotensin II synthesis by captopril on the response of plasma ADH to the osmotic and volume-dependent stimuli has been studied in 15 uremic patients. Captopril administration had no effect either on basal plasma ADH or on plasma ADH response to the osmotic stimulus. Time-course of plasma ADH following hypertonic saline administration and sensitivity of the response (increase of plasma ADH related to increase of plasma sodium) were not modified. On the contrary, the response of plasma ADH to the volume-dependent stimulus induced by hemofiltration was markedly blunted by captopril administration. The sensitivity estimated from the slope of the regression line relating plasma ADH to the cumulated lost volume was clearly diminished. These results suggest that angiotensin II mediates ADH response only to the volume-dependent stimulus.
我们对15例尿毒症患者研究了卡托普利抑制血管紧张素II合成对血浆抗利尿激素（ADH）对渗透压和容量依赖性刺激反应的影响。给予卡托普利对基础血浆ADH或血浆ADH对渗透压刺激的反应均无影响。给予高渗盐水后血浆ADH的时间进程以及反应的敏感性（血浆ADH的增加与血浆钠增加相关）均未改变。相反，给予卡托普利使血浆ADH对血液滤过诱导的容量依赖性刺激的反应明显减弱。根据将血浆ADH与累积失液量相关的回归线斜率估算的敏感性明显降低。这些结果表明，血管紧张素II仅介导ADH对容量依赖性刺激的反应。
