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首页> 外文期刊>Physiological Reviews >Mouse models and the urinary concentrating mechanism in the new millennium.
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Mouse models and the urinary concentrating mechanism in the new millennium.

机译：新千年的小鼠模型和尿液浓缩机制。

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Our understanding of urinary concentrating and diluting mechanisms at the end of the 20th century was based largely on data from renal micropuncture studies, isolated perfused tubule studies, tissue analysis studies and anatomical studies, combined with mathematical modeling. Despite extensive data, several key questions remained to be answered. With the advent of the 21st century, a new approach, transgenic and knockout mouse technology, is providing critical new information about urinary concentrating processes. The central goal of this review is to summarize findings in transgenic and knockout mice pertinent to our understanding of the urinary concentrating mechanism, focusing chiefly on mice in which expression of specific renal transporters or receptors has been deleted. These include the major renal water channels (aquaporins), urea transporters, ion transporters and channels (NHE3, NKCC2, NCC, ENaC, ROMK, ClC-K1), G protein-coupled receptors (type 2 vasopressin receptor, prostaglandin receptors,endothelin receptors, angiotensin II receptors), and signaling molecules. These studies shed new light on several key questions concerning the urinary concentrating mechanism including: 1) elucidation of the role of water absorption from the descending limb of Henle in countercurrent multiplication, 2) an evaluation of the feasibility of the passive model of Kokko-Rector and Stephenson, 3) explication of the role of inner medullary collecting duct urea transport in water conservation, 4) an evaluation of the role of tubuloglomerular feedback in maintenance of appropriate distal delivery rates for effective regulation of urinary water excretion, and 5) elucidation of the importance of water reabsorption in the connecting tubule versus the collecting duct for maintenance of water balance.
机译：我们对20世纪末的尿液浓缩和稀释机制的理解主要基于肾脏微穿刺研究，孤立的灌注小管研究，组织分析研究和解剖学研究的数据，并结合了数学建模。尽管有大量数据，但仍有几个关键问题需要回答。随着21世纪的到来，一种新的方法，即转基因和敲除小鼠技术，正在提供有关尿液浓缩过程的重要新信息。这篇综述的主要目的是总结与我们对尿液浓缩机制的了​​解有关的转基因和基因敲除小鼠的发现，主要集中在已删除特定肾脏转运蛋白或受体表达的小鼠上。这些包括主要的肾脏水通道（水通道蛋白），尿素转运蛋白，离子转运蛋白和通道（NHE3，NKCC2，NCC，ENaC，ROMK，ClC-K1），G蛋白偶联受体（2型加压素受体，前列腺素受体，内皮素受体） ，血管紧张素II受体）和信号分子。这些研究为有关尿液浓缩机制的几个关键问题提供了新的思路，其中包括：1）阐明Henle的下肢吸水在逆流增殖中的作用，2）评价Kokko-Rector被动模型的可行性和Stephenson，3）阐述了髓内收集导管尿素运输在节水中的作用，4）评估肾小管肾反馈在维持适当的远端输液速率以有效调节尿液排泄中的作用，以及5）阐明对于保持水平衡，在连接小管和收集管中重新吸收水的重要性。

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