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Articles in PresS, published online ahead of print November 26, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00234.2002
Submitted on June 24, 2002
Accepted on November 18, 2002
1 University of Aarhus, The Water and Salt Research Center, 8000 Aarhus, Denmark; University of Aarhus, Institute of Anatomy, 8000 Aarhus, Denmark
2 University of Aarhus, The Water and Salt Research Center, 8000 Aarhus, Denmark; University of Aarhus, Institute of Experimental Clinical Research, 8000 Aarhus, Denmark
* To whom correspondence should be addressed. E-mail: sn{at}ana.au.dk.
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 dDAVP treatment (2 hrs) 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 V2-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 V2-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.
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