Renal expression of aquaporins in liver cirrhosis induced by chronic common bile duct ligation in rats.

Renal expression of aquaporins in liver cirrhosis induced by chronic common bile duct ligation in rats.
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发表时间:
1999-09
期刊:
Journal of the American Society of Nephrology : JASN
影响因子:
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通讯作者:
P. Fernández-Llama;R. Turner;G. Dibona;M. Knepper
P. Fernández-Llama;R. Turner;G. Dibona;M. Knepper
中科院分区:
其他
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作者:
P. Fernández-Llama;R. Turner;G. Dibona;M. Knepper

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采用半定量免疫印迹法检测胆总管结扎(CBDL)继发性肝硬化大鼠肾脏中四种主要肾水通道蛋白、粗升肢Na-K-2Cl协同转运蛋白、3型Na-H交换器和Na-K-ATP酶的表达水平。这些大鼠有明显的水潴留和低钠血症。与四氯化碳诱导的肝硬化模型相比,CBDL诱导的肝硬化中水通道蛋白-2的表达降低。因此,这些结果表明,在细胞外液容量扩张的情况下,在水通道蛋白-2丰度不增加的情况下,可能会发生过度保水和低钠血症。此外,与假手术对照大鼠相比,CBDL 大鼠中两种基底外侧集合管水通道蛋白(aquaporin-3 和 -4)的表达水平降低。类似地,粗升肢的 Na-K-2Cl 协同转运蛋白和 3 型 Na-H 交换蛋白表现出表达减少。相反,水通道蛋白-1和Na-K-ATP酶所有亚基的表达水平没有降低。因此,多个水通道和离子转运蛋白的失调可能在与 CBDL 诱导的大鼠肝硬化相关的水平衡异常中发挥作用。
Semiquantitative immunoblotting was used to investigate the expression levels of the four major renal aquaporins, the Na-K-2Cl cotransporter of the thick ascending limb, the type 3 Na-H exchanger, and the Na-K-ATPase in kidneys from rats with cirrhosis secondary to common bile duct ligation (CBDL). These rats had significant water retention and hyponatremia. In contrast to models of cirrhosis induced by carbon tetrachloride, aquaporin-2 expression in CBDL-induced cirrhosis was decreased. Thus, these results show that in the setting of extracellular fluid volume expansion, excessive water retention with hyponatremia can occur in the absence of increases in aquaporin-2 abundance. In addition, the expression levels of the two basolateral collecting duct aquaporins (aquaporin-3 and -4) were decreased in CBDL rats relative to sham-operated control rats. Similarly, the Na-K-2Cl cotransporter of the thick ascending limb and the type 3 Na-H exchanger showed decreases in expression. In contrast, the expression levels of aquaporin-1 and the all subunit of the Na-K-ATPase were not decreased. Thus, dysregulation of multiple water channels and ion transporters may play a role in water balance abnormalities associated with CBDL-induced cirrhosis in rats.