Schou Morten, Gabrielsen Anders, Bruun Niels Eske, Skøtt Peter, Pump Bettina, Dige-Petersen Harriet, Frandsen Erik, Bie Peter, Warberg Jørgen, Christensen Niels Juel, Norsk Peter
Department of Aviation Medicine, The Heart Centre, The National University Hospital (Rigshospitalet) Dept. 7522, 9 Blegdamsvej, DK-2100 Copenhagen, Denmark.
Am J Physiol Regul Integr Comp Physiol. 2002 Jul;283(1):R187-96. doi: 10.1152/ajpregu.00536.2001.
The hypothesis was tested that suppression of generation of ANG II is one of the mechanisms of the water immersion (WI)-induced natriuresis in humans. In one protocol, eight healthy young males were subjected to 3 h of 1) WI (WI + placebo), 2) WI combined with ANG II infusion of 0.5 ng. kg(-1). min(-1) (WI + ANG II-low), and 3) a seated time control (Con). In another almost identical protocol, 7-10 healthy young males were investigated to delineate the tubular site(s) of action of ANG II by the lithium clearance method (C(Li)) and were on an additional fourth study day subjected to infusion of ANG II at a rate of 1.5 ng. kg(-1). min(-1) (WI + ANG II-high). During WI + placebo, plasma concentration of ANG II decreased from 16 +/- 2 to 8 +/- 1 pg/ml (P < 0.05) and renal sodium excretion increased from 104 +/- 15 to 294 +/- 27 micromol/min (P < 0.05). During WI + ANG II-low, plasma ANG II was not suppressed by WI, and the natriuresis was blunted by 52 +/- 13% (P < 0.05). During WI + ANG II-low and WI + ANG II-high, an increase in C(Li) was prevented that was otherwise observed during WI, and fractional distal reabsorption of sodium was facilitated. In conclusion, maintaining plasma concentration of ANG II unchanged at the level of control attenuates the natriuresis of WI considerably in humans. Therefore, suppression of generation of ANG II is an important mechanism of the natriuresis of WI in humans. Furthermore, infusion of ANG II during WI prevents an otherwise induced increase in C(Li) and facilitates the fractional distal reabsorption of sodium, probably via an effect on aldosterone release.
抑制血管紧张素II（ANG II）的生成是水浸（WI）诱导人体利钠的机制之一。在一个实验方案中，八名健康年轻男性接受了3小时的以下处理：1）水浸（WI + 安慰剂）；2）水浸联合0.5 ng·kg⁻¹·min⁻¹的ANG II输注（WI + ANG II - 低剂量）；3）坐位时间对照（Con）。在另一个几乎相同的实验方案中，7 - 10名健康年轻男性通过锂清除率方法（C(Li)）来确定ANG II的肾小管作用部位，并在另外的第四个研究日接受1.5 ng·kg⁻¹·min⁻¹的ANG II输注（WI + ANG II - 高剂量）。在WI + 安慰剂期间，ANG II的血浆浓度从16 ± 2 pg/ml降至8 ± 1 pg/ml（P < 0.05），肾钠排泄从104 ± 15 μmol/min增加到294 ± 27 μmol/min（P < 0.05）。在WI + ANG II - 低剂量期间，WI未抑制血浆ANG II，利钠作用减弱了52 ± 13%（P < 0.05）。在WI + ANG II - 低剂量和WI + ANG II - 高剂量期间，WI期间原本会出现的C(Li)增加被阻止，并且促进了钠的远端分数重吸收。总之，将ANG II的血浆浓度维持在对照水平不变可显著减弱人体WI的利钠作用。因此，抑制ANG II的生成是人体WI利钠的重要机制。此外，WI期间输注ANG II可防止原本诱导的C(Li)增加，并促进钠的远端分数重吸收，这可能是通过对醛固酮释放的影响实现的。
