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Am J Physiol Renal Physiol (July 16, 2002). doi:10.1152/ajprenal.00207.2002
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Articles in PresS, published online ahead of print July 16, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00207.2002
Submitted on June 3, 2002
Accepted on July 11, 2002

A rat kidney tubule suspension for the study of vasopressin-induced shuttling of aquaporin-2 water channels

Stephen Shaw1 and David Marples1*

1 School of Biomedical Sciences, University of Leeds, Leeds, W. Yorkshire, United Kingdom

* To whom correspondence should be addressed. E-mail: phsddrm{at}leeds.ac.uk.

Vasopressin (AVP) increases the osmotic water permeability of the renal collecting ducts by inducing the translocation of specific aquaporin-2 (AQP2) water channels from cytoplasmic vesicles to the apical plasma membrane of the principal cells. Here we report a novel inner medullary tubule suspension for the study of this phenomenon, which overcomes some of the drawbacks faced by current techniques; both primary cultures of inner medullary collecting duct cells and cell lines expressing AQP2 show aberrant trafficking and/or signalling pathways. The tubule suspensions were prepared by proteolytic digestion of inner medullae dissected from freshly isolated rat kidneys. Following drug treatment cellular distribution of AQP2 was determined by membrane fractionation and Western blotting, or immunocytochemistry. Treatment of suspensions with 1 nM AVP caused redistribution of AQP2 to the apical plasma membrane of the principal cells, a process inhibited by microtubule disruption or protein kinase A inhibition. We conclude that this method provides a valuable new approach to the study of the cellular mechanisms involved in the response of the collecting duct to AVP.




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