Christensen Birgitte Mønster, Wang Weidong, Frøkiaer Jørgen, Nielsen Søren
The Water and Salt Research Center, Institute of AnatomyUniversity of DK-8000 Aarhus, Denmark.
Am J Physiol Renal Physiol. 2003 Apr;284(4):F701-17. doi: 10.1152/ajprenal.00234.2002. Epub 2002 Nov 26.
The purpose of the present study was to examine whether there is axial heterogeneity in the basolateral plasma membrane (BLM) localization of AQP2 and whether altered vasopressin action or medullary tonicity affects the BLM localization of AQP2. Immunocytochemistry and immunoelectron microscopy revealed AQP2 labeling of the BLM in connecting tubule (CNT) cells and inner medullary collecting duct (IMCD) principal cells in normal rats and vasopressin-deficient Brattleboro rats. In contrast there was little basolateral AQP2 labeling in cortical (CCD) and outer medullary collecting duct principal cells. Short-term desamino-Cys(1), (D)-Arg(8) vasopressin (dDAVP) treatment (2 h) of Brattleboro rats caused no increase in AQP2 labeling of the BLM. In contrast, long-term dDAVP treatment (6 days) of Brattleboro rats caused an increased BLM labeling in CNT, CCD, and IMCD. Treatment of normal rats with V(2)-receptor antagonist for 60 min caused retrieval of AQP2 from the apical plasma membrane. Moreover, AQP2 labeling of the BLM was unchanged in CNT and IMCD but increased in CCD. In conclusion, there is an axial heterogeneity in the subcellular localization of AQP2 with prominent AQP2 labeling of the BLM in CNT and IMCD. There was no increase in AQP2 labeling of the BLM in response to short-term dDAVP. Moreover, acute V(2)-receptor antagonist treatment did not cause retrieval of AQP2 from the BLM. In contrast, long-term dDAVP treatment caused a major increase in AQP2 expression in the BLM in CCD.
本研究的目的是检测水通道蛋白2（AQP2）在基底外侧质膜（BLM）的定位是否存在轴向异质性，以及血管加压素作用的改变或髓质张力是否会影响AQP2在BLM的定位。免疫细胞化学和免疫电子显微镜显示，正常大鼠和血管加压素缺乏的布拉特洛伯大鼠的连接小管（CNT）细胞和内髓集合管（IMCD）主细胞的BLM有AQP2标记。相比之下，皮质集合管（CCD）和外髓集合管主细胞的基底外侧AQP2标记很少。对布拉特洛伯大鼠进行短期去氨基半胱氨酸（1），（D）-精氨酸（8）血管加压素（dDAVP）治疗（2小时），并未使BLM的AQP2标记增加。相反，对布拉特洛伯大鼠进行长期dDAVP治疗（6天），导致CNT、CCD和IMCD中BLM标记增加。用V2受体拮抗剂处理正常大鼠60分钟，导致AQP2从顶端质膜回收。此外，CNT和IMCD中BLM的AQP2标记未改变，但CCD中增加。总之，AQP2的亚细胞定位存在轴向异质性，CNT和IMCD中BLM有明显的AQP2标记。短期dDAVP处理后，BLM的AQP2标记未增加。此外，急性V2受体拮抗剂处理未导致AQP2从BLM回收。相反，长期dDAVP治疗导致CCD中BLM的AQP2表达大幅增加。
