CLC-K1, a kidney-specific chloride channel, has been demonstrated to be involved in the urine concentration mechanism. Here, we investigated the developmental expression of CLC-K1 in the rat kidney. Using immunohistochemistry, we showed that CLC-K1 was not present in the thin ascending limb of Henle's loop during the early prenatal stages but was significantly expressed during the adult stage. CLC-K1 started to appear at day 5 and its expression increased during further development. In developing rats this increase coincided with the increase in the urine-concentrating capacity as the animals matured. We also investigated the expressions of other channels and transporters, including NKCC2, AQP-1, and AQP-2. NKCC2 was strongly expressed throughout the inner medulla in neonatal rat kidneys but was entirely undetectable at the adult stage. The decline in its expression took the form of a gradual recession from the inner medulla together with reciprocal increases in the expression of CLC-K1. AQP-1 was weakly expressed in the inner medulla during early development and showed a rapid increase in expression at a later stage. The collecting duct cells significantly expressed AQP-2 even at birth and maintained its expression throughout the development. These results suggest that CLC-K1 expression is one of the major determinants of the urine-concentrating capacity of the developing rat kidney.

中文翻译：

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CLC-K1在出生后大鼠肾脏中的发育表达。

已经证明，CLC-K1是肾脏特异性的氯离子通道，与尿液浓缩机制有关。在这里，我们调查了大鼠肾脏中CLC-K1的发育表达。使用免疫组织化学，我们显示CLC-K1在产前早期在Henle环的细小上升肢中不存在，但在成年期中明显表达。CLC-K1在第5天开始出现，其表达在进一步发展过程中增加。在发育中的大鼠中，随着动物的成熟，这种增加与尿液浓缩能力的增加相吻合。我们还研究了其他通道和转运蛋白的表达，包括NKCC2，AQP-1和AQP-2。NKCC2在新生大鼠肾脏的整个髓质中强烈表达，但在成年期则完全未检测到。其表达的下降采取了从内髓逐渐衰退的形式，同时CLC-K1的表达也相应增加。在早期发育过程中，AQP-1在内侧髓质中表达较弱，而在后期则表达迅速增加。收集导管细胞甚至在出生时就显着表达AQP-2，并在整个发育过程中保持其表达。这些结果表明，CLC-K1表达是发育中大鼠肾脏尿液浓缩能力的主要决定因素之一。收集导管细胞甚至在出生时就显着表达AQP-2，并在整个发育过程中保持其表达。这些结果表明，CLC-K1表达是发育中大鼠肾脏尿液浓缩能力的主要决定因素之一。收集导管细胞甚至在出生时就显着表达AQP-2，并在整个发育过程中保持其表达。这些结果表明，CLC-K1表达是发育中大鼠肾脏尿液浓缩能力的主要决定因素之一。