AJP - Renal Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Renal Physiol 297: F10-F18, 2009. First published February 25, 2009; doi:10.1152/ajprenal.00053.2009
0363-6127/09 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
297/1/F10    most recent
00053.2009v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (1)
Google Scholar
Right arrow Articles by Hasler, U.
Right arrow Articles by Féraille, E.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hasler, U.
Right arrow Articles by Féraille, E.

REVIEW

Aquaporin-2 abundance in the renal collecting duct: new insights from cultured cell models

Udo Hasler, Valérie Leroy, Pierre-Yves Martin, and Eric Féraille

Service de Néphrologie, Fondation pour Recherches Médicales, University of Geneva, Geneva, Switzerland

Submitted 2 February 2009 ; accepted in final form 20 February 2009

ABSTRACT

The renal cortico-papillary osmotic gradient is generated by sodium reabsorption in the thick ascending limb. The antidiuretic hormone arginine vasopressin (AVP) increases collecting duct water permeability by enhancing aquaporin-2 (AQP2) water channel insertion in the apical membrane of principal cells, allowing water to passively flow along the osmotic gradient from the tubule lumen to the interstitium. In addition to short-term AQP2 redistribution between intracellular compartments and the cell surface, AQP2 whole cell abundance is tightly regulated. AVP is a major transcriptional activator of the AQP2 gene, and stimulation of insulin- and calcium-sensing receptors respectively potentiate and reduce its action. Extracellular tonicity is another key factor that determines the levels of AQP2 abundance. Its effect is dependent on activation of the tonicity-responsive enhancer binding protein that reinforces AVP-induced AQP2 transcriptional activation. Conversely, activation of the NF-{kappa}B transcriptional factor by proinflammatory factors reduces AQP2 gene transcription. Aldosterone additionally regulates AQP2 whole cell abundance by simultaneously reducing AQP2 gene transcription and stimulating AQP2 mRNA translation. These examples illustrate how cross talk between various stimuli regulates AQP2 abundance in collecting duct principal cells and consequently contributes to maintenance of body water homeostasis.

water transport; osmolality; vasopressin



Address for reprint requests and other correspondence: Eric Féraille, Service de Néphrologie, Fondation pour Recherches Médicales, 64 Ave. de la Roseraie, 1211 Geneva 4, Switzerland (e-mail: eric.feraille{at}unige.ch)




This article has been cited by other articles:


Home page
Am. J. Physiol. Renal Physiol.Home page
K. J. Bergsland, F. L. Coe, D. L. Gillen, and E. M. Worcester
A test of the hypothesis that the collecting duct calcium-sensing receptor limits rise of urine calcium molarity in hypercalciuric calcium kidney stone formers
Am J Physiol Renal Physiol, October 1, 2009; 297(4): F1017 - F1023.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2009 by the American Physiological Society.