Decreased expression of aquaporin 2 in the collecting duct of mice lacking the vasopressin V1a receptor
Decreased expression of aquaporin 2 in the collecting duct of mice lacking the vasopressin V1a receptor
复制标题
缺乏加压素 V1a 受体的小鼠集合管中水通道蛋白 2 的表达降低
DOI：
10.1007/s10157-012-0686-3
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发表时间：
2013
期刊：
影响因子：
2.3
通讯作者：
Kawahara K
中科院分区：
文献类型：
--
作者：
Yasuoka Y;Kobayashi M;Sato Y;Nonoguchi H;Tanoue A;Okamoto H;Kawahara K
背景加压素V1 a受体缺失（V1 aR-/-）小鼠最近由于在对照和水利尿（正常水合）期间的较高尿量而显示不完全的尿浓缩，但在脱水期间显示正常反应（Aoyagi等，第295章：一个人F100-7，2008）。方法因此，使用改进的尿液收集方法进一步检查野生型（WT）和V1 aR −/−小鼠肾脏中的水平衡、血浆加压素、血浆和尿液渗透压以及水通道蛋白2（AQP 2）表达结果V1 aR −/−小鼠表现出较低的尿渗透压（3，360 ± 138 vs.3，610 ± 47 mOsm/kgH 2 O）和更高的血浆渗透压（354.3 ± 1.3 vs.342.5 ± 1.5 mOsm/kgH 2 O）（P< 0.05）。相比之下，V1 aR −/−小鼠的血浆加压素浓度显著（P< 0.001）更高（48.8 ± 4.8 vs. 22.1 ± 2.4 pg/ml）。另一方面，虽然肾脏中的AQP 2蛋白表达在脱水后增加，但V1 aR −/−小鼠中的基础（对照）和脱水诱导的AQP 2蛋白水平与WT小鼠相比显著降低（通过Western印迹法）。脱水后，V1 aR −/−和WT小鼠集合管管腔膜中的抗AQP 2抗体染色增加，但V1 aR −/−小鼠中的染色相对较弱（通过免疫组织化学）。结论V1 aR信号通路可能是控制条件和脱水条件下集合管AQP 2表达的重要机制。
BackgroundVasopressin V1a receptor null (V1aR−/−) mice recently showed incomplete urinary concentration due to higher urine volume during control and water diuresis (euhydration), but showed normal response during dehydration (Aoyagi et al., Am J Physiol 295: F100–7, 2008).MethodsWater balance, plasma vasopressin, plasma and urine osmolality, and aquaporin 2 (AQP2) expression in the kidney of wild-type (WT) and V1aR−/−mice were therefore further examined using improved methods of urine collection (urinary bladder urine).ResultsV1aR−/−mice demonstrated a lower urine osmolality (3,360 ± 138 vs. 3,610 ± 47 mOsm/kgH2O) and a higher plasma osmolality (354.3 ± 1.3 vs. 342.5 ± 1.5 mOsm/kgH2O) after dehydration for 24 h compared to WT mice (P< 0.05). In contrast, the plasma vasopressin concentration was significantly (P< 0.001) higher in the V1aR−/−mice (48.8 ± 4.8 vs. 22.1 ± 2.4 pg/ml). On the other hand, although the AQP2 protein expression in the kidney was increased after dehydration, the basal (control) and dehydration-induced AQP2 protein levels were significantly lower in V1aR−/−mice compared to WT mice (by Western blotting). Staining by an anti-AQP2 antibody in the luminal membrane of the collecting ducts was increased in both V1aR−/−and WT mice after dehydration, but was relatively weaker in the V1aR−/−mice (by immunohistochemistry). Moreover, urinary excretion of AQP2 protein, an index of the luminal AQP2 expression, was significantly (P< 0.05) lower in the V1aR−/−mice.ConclusionV1aR signaling may be fundamentally important for the expression of AQP2 in the collecting ducts during control conditions and dehydration.