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脱水过程中衰老肾脏和大脑中尿素转运蛋白的表达

Urea transporter expression in aging kidney and brain during dehydration.

作者信息

Trinh-Trang-Tan M-M, Geelen G, Teillet L, Corman B

机构信息

Institut National de la Santé et de la Recherche Médicale U76, Institut National de Transfusion Sanguine, 6, rue Alexandre Cabanel, F-75015 Paris, France.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2003 Dec;285(6):R1355-65. doi: 10.1152/ajpregu.00207.2003. Epub 2003 Aug 21.

DOI:10.1152/ajpregu.00207.2003
PMID:12933359
Abstract

Aging is commonly associated with defective urine-concentrating ability. The present study examined how the kidney and the brain of senescent (30-mo-old) female WAG/Rij rats respond to dehydration induced by 2 days of water deprivation in terms of urea transporter (UT) regulation. In euhydrated situation, senescent rats exhibited similar vasopressin plasma level but lower urine osmolality and papillary urea concentration and markedly reduced kidney UT-A1, UT-A3, and UT-B1 abundances compared with adult (10-mo-old) rats. Senescent rats responded to dehydration similarly to adult rats by a sixfold increase in vasopressin plasma level. Their papillary urea concentration was doubled, without, however, attaining that of dehydrated adult rats. Such an enhanced papillary urea sequestration occurred with a great fall of both UT-A1 and UT-A3 abundances in the tip of inner medulla and an increased UT-A1 abundance in the base of inner medulla. UT-A2 and UT-B1 were unchanged. These data suggest that the inability of control and thirsted senescent rats to concentrate urine as much as their younger counterparts derives from lower papillary urea concentration. In aging brain, UT-B1 abundance was increased twofold together with a fourfold increase in aquaporin-4 abundance. Dehydration did not alter the abundance of these transporters.

摘要

衰老通常与尿液浓缩能力缺陷有关。本研究考察了衰老(30月龄)雌性WAG/Rij大鼠的肾脏和大脑在尿素转运体(UT)调节方面如何应对2天禁水诱导的脱水。在正常水合状态下,与成年(10月龄)大鼠相比,衰老大鼠的血浆血管加压素水平相似,但尿渗透压和乳头尿素浓度较低,肾脏UT-A1、UT-A3和UT-B1丰度显著降低。衰老大鼠对脱水的反应与成年大鼠相似,血浆血管加压素水平增加了六倍。它们的乳头尿素浓度增加了一倍,但未达到脱水成年大鼠的水平。这种乳头尿素潴留增强伴随着内髓质尖端UT-A1和UT-A3丰度的大幅下降以及内髓质基部UT-A1丰度的增加。UT-A2和UT-B1没有变化。这些数据表明,对照和脱水的衰老大鼠不能像年轻大鼠那样浓缩尿液,原因是乳头尿素浓度较低。在衰老的大脑中,UT-B1丰度增加了两倍,水通道蛋白-4丰度增加了四倍。脱水并未改变这些转运体的丰度。

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