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首页> 外文期刊>American Journal of Physiology >Angiotensin II attenuates the natriuresis of water immersion in humans.
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Angiotensin II attenuates the natriuresis of water immersion in humans.

机译：血管紧张素II减弱了浸入人体的利尿作用。

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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.
机译：检验了该假设，即抑制ANG II的产生是人类水浸（WI）引起的利尿机制之一。在一种方案中，对八名健康的年轻男性进行3小时的1）WI（WI +安慰剂），2）WI联合0.5 ng ANG II输注。千克（-1）。 min（-1）（WI + ANG II-low），以及3）座位时间控制（Con）。在另一个几乎相同的方案中，研究了7-10名健康的年轻男性，通过锂清除法（C（Li））描绘了ANG II的管状部位，并在另外的第4个研究日接受了ANG II的速率为1.5 ng。千克（-1）。 min（-1）（WI + ANG II高）。在WI +安慰剂治疗期间，ANG II的血浆浓度从16 +/- 2降低到8 +/- 1 pg / ml（P <0.05），并且肾脏钠排泄从104 +/- 15微摩尔/增加到294 +/- 27微摩尔/毫升。分钟（P <0.05）。在WI + ANG II低时，WI不能抑制血浆ANG II，并且利尿剂变钝52 +/- 13％（P <0.05）。在WI + ANG II低和WI + ANG II高时，可防止WI期间观察到的C（Li）升高，并促进远端钠的部分重吸收。总之，在控制水平上保持ANG II的血浆浓度不变会大大减轻人的WI的利尿作用。因此，抑制ANGII的产生是人类WI中钠尿的重要机制。此外，在WI期间输注ANG II可能会阻止其他方面引起的C（Li）升高，并促进钠的部分远侧重吸收，这可能是通过对醛固酮的释放造成的。

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