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首页> 外文期刊>American Journal of Physiology >Lack of UT-B in vasa recta and red blood cells prevents urea-induced improvement of urinary concentrating ability.
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Lack of UT-B in vasa recta and red blood cells prevents urea-induced improvement of urinary concentrating ability.

机译：血管直肠和红细胞缺乏UT-B会阻止尿素诱导的尿液浓缩能力的提高。

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摘要

Recycling of urea within the renal medulla is known to play an important role in the capacity of the kidney to concentrate urine. This recycling occurs simultaneously through a tubular and a vascular route (i.e., through the loops of Henle and vasa recta, respectively). In the present study, transgenic mice with a selective deficiency in UT-B (the urea transporter protein expressed in descending vasa recta and red blood cells), were used to evaluate the specific contribution of vascular urea recycling to overall urine-concentrating ability (UCA). The renal handling of urea was studied in normal conditions and after acute or chronic alterations in urea excretion (acute urea loading or variations in protein intake, respectively). In normal conditions, UT-B null mice exhibited a 44% elevation in plasma urea (Purea), a normal creatinine clearance, but a 25% decrease in urea clearance, with no change in that of sodium and potassium. Acute urea loading induced a progressive increase in urinary urea concentration (Uurea) in wild-type mice and a subsequent improvement in their UCA in contrast to UT-B null mice, in which urinary osmolality and Uurea did not rise, due to the failure to accumulate urea in the medulla. With increasing protein intake (from 10 to 40% protein in diet, leading to a 5-fold increase in urea excretion), Purea was further increased in null mice while little change was observed in wild-type mice, and null mice were not able to increase Uurea as did wild-type mice. In conclusion, this study in UT-B-deficient mice reveals that countercurrent exchange of urea in renal medullary vessels and red blood cells accounts for a major part of the kidney's concentrating ability and for the adaptation of renal urea handling during a high-protein intake.
机译：已知肾髓质内尿素的再循环在肾脏浓缩尿液的能力中起着重要作用。这种再循环通过管状和血管途径同时发生（即分别通过Henle和vasa recta的回路）。在本研究中，使用具有选择性缺陷的UT-B（降落的血管直肠和红细胞中表达的尿素转运蛋白）的转基因小鼠来评估血管尿素回收对总体尿液浓缩能力（UCA）的特定贡献。 ）。在正常情况下以及尿素排泄的急性或慢性改变（分别为急性尿素负荷或蛋白质摄入量变化）后，研究了肾脏对尿素的处理。在正常情况下，无UT-B的小鼠血浆尿素（Purea）升高44％，肌酐清除率正常，但尿素清除率降低25％，而钠和钾的含量无变化。急性尿素负荷导致野生型小鼠尿素浓度（Uurea）逐渐增加，而其UCA则有所改善，这与UT-B无效小鼠相反，由于尿素摩尔渗透压和尿素浓度没有升高，UT-B无效尿素在髓质中积累。随着蛋白质摄入量的增加（饮食中蛋白质含量从10％增加到40％，导致尿素排泄增加5倍），无效小鼠中的Purea进一步增加，而野生型小鼠中观察到的变化很小，无效小鼠则无法与野生型小鼠一样增加尿素。总而言之，这项针对UT-B缺陷小鼠的研究表明，肾髓质血管和红细胞中尿素的逆流交换是肾脏浓缩能力的主要部分，也是高蛋白摄入期间肾脏对尿素处理的适应性改变。 。

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