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首页> 外文期刊>American Journal of Physiology >Downregulation of AQP1, -2, and -3 after ureteral obstruction is associated with a long-term urine-concentrating defect.
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Downregulation of AQP1, -2, and -3 after ureteral obstruction is associated with a long-term urine-concentrating defect.

机译：输尿管梗阻后AQP1，-2和-3的下调与长期尿液浓缩缺陷有关。

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摘要

Previously, we demonstrated that 24 h of bilateral ureteral obstruction (BUO) and short-term release of BUO was associated with a decrease in the expression of aquaporin-2 (AQP2), polyuria, and a reduced urinary concentrating capacity (10). The purposes of the present study were to examine whether BUO and the long-term release of BUO (BUO-R) for 3, 14, and 30 days were associated with changes in the expression of renal AQP1, AQP2, and AQP3 and whether such changes were associated with parallel changes in urinary output and urinary concentrating capacity. Rats (n = 4-7 in each group) were kept in metabolic cages for measurements of urinary output. Kidneys were removed to determine the expression levels of AQP1, AQP2, and AQP3 by semiquantitative immunoblotting. AQP2 was downregulated after 24 h of BUO (42 +/- 3%). Downregulation of AQP2 persisted 3 (43 +/- 14%; P < 0.01) and 15 days after BUO-R (48 +/- 11%; P < 0.01) but was normalized 30 days after BUO-R. AQP3 showed a similar pattern. Moreover, AQP1 was downregulated in response to BUO (65 +/- 7%) and remained downregulated 3 days after BUO-R (41 +/- 5%), 14 days after BUO-R (57 +/- 8%), and 30 days after BUO-R (59 +/- 5%). BUO-R resulted in a significant polyuria that gradually decreased, although it remained significant at day 30. Urinary concentrating capacity remained significantly impaired when determined 3, 14, and 30 days after BUO-R in response to a 24-h period of thirst (1,712 +/- 270 vs. 2,880 +/- 91 mosmol/kgH2O at day 30, P < 0.05). In conclusion, the expression of AQP1, AQP2, and AQP3 were long-term downregulated after BUO-R, suggesting that dysregulation of aquaporins located at the proximal tubule, thin descending limb of the loop of Henle, and the collecting duct may contribute to the long-term polyuria and impairment of urinary concentrating capacity associated with obstructive nephropathy.
机译：以前，我们证明双侧输尿管梗阻（BUO）和BUO的短期释放24小时与aquaporin-2（AQP2）的表达减少，多尿症和尿液浓缩能力降低有关（10）。本研究的目的是检查BUO和BUO在3、14和30天的长期释放是否与肾AQP1，AQP2和AQP3表达的变化有关，以及是否这些变化与尿量和尿液浓缩能力的平行变化有关。将大鼠（每组n ＝ 4-7）关在代谢笼中以测量尿量。通过半定量免疫印迹法去除肾脏以确定AQP1，AQP2和AQP3的表达水平。 BUO 24小时后（42 +/- 3％）AQP2下调。 AQP2的下调在BUO-R后持续3天（43 +/- 14％; P <0.01）和15天（48 +/- 11％; P <0.01）持续存在，但在BUO-R后30天得以正常化。 AQP3显示了类似的模式。此外，AQP1因BUO而下调（65 +/- 7％），并在BUO-R后3天（41 +/- 5％），在BUO-R后14天（57 +/- 8％）保持下调， BUO-R（59 +/- 5％）后30天。 BUO-R导致明显的多尿症，尽管在第30天仍显着，但逐渐减少。尿液浓缩能力在BUO-R后第3、14和30天测定，以响应24小时的口渴时，尿浓缩能力仍然明显受损（第30天时为1,712 +/- 270 vs.2,880 +/- 91 mosmol / kgH2O，P <0.05）。总之，在BUO-R后，AQP1，AQP2和AQP3的表达长期下调，表明位于近端小管，Henle环的薄降肢和收集管的水通道蛋白失调可能有助于长期多尿症和与梗阻性肾病相关的尿液浓缩能力受损。

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