Urea and urine concentrating ability in mice lacking AQP3
- VernacularTitle:AQP3缺失小鼠尿素和尿浓缩能力的研究
- Author:
Jianguo ZHU
;
Xichun LIU
;
Xuejian ZHAO
;
Dan ZHAO
- Publication Type:Journal Article
- Keywords:
Transgenic mouse;
Urea transport;
Aquaporin 3;
Urea
- From:
Chinese Journal of Pathophysiology
2009;25(11):2136-2140
- CountryChina
- Language:Chinese
-
Abstract:
AIM: Aquaporin 3 ( AQP3 ) water channel expressed in the kidney plays a critical role in the urine concentrating mechanism. Mice with AQP3 deletion show a urinary concentrating defect. To better characterize this defect, we studied the influence and mechanism of an acute urea load in conscious AQP3 - null and wild - type mice. METHODS:Urine was collected and assayed every 2 h, from 2 h before (baseline) to 8 h after the urea load. Urine volume, urine osmolality and urea concentration were measured. RNA was isolated from the whole kidney and real - time PCR was carried out using a LightCycler. Total protein of UTs was assayed from kidney tissue by Western blotting. RESULTS: Mice of both genotypes excreted the urea loaded in ～ 4 h with the same time course. Despite their low baseline, the AQP3 - null mice raised their urine osmolality and urea concentration progressively after the urea load to the values almost equal to those in wild - type mice at 8 h. In contrast, urine non - urea solute concentration did not change. Urine volume fell in the last 4 h to about one - fourth of basal values. The urea load strongly upregulated urea transporter UT - A3 expression in both genotype mice. CONCLUSION: These observations show that lack of AQP3 does not interfere with the ability of the kidney to concentrate urea but impairs its ability to concentrate other solutes. This solute - selective response results from the capacity of AQP3 to transport not only water but also urea, suggesting a novel role for AQP3 in non - urea solute concentration in the urine.
