HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 294/3/F582    most recent 00427.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Galizia, L. Articles by Ford, P. Search for Related Content PubMed PubMed Citation Articles by Galizia, L. Articles by Ford, P.

Role of AQP2 in activation of calcium entry by hypotonicity: implications in cell volume regulation

Laboratorio de Biomembranas, Departamento de Fisiología y Biofísica, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina

Submitted 11 September 2007 ; accepted in final form 14 December 2007

We previously reported in a rat cortical collecting duct cell line (RCCD₁) that the presence of aquaporin 2 (AQP2) in the cell membrane is critical for the rapid activation of regulatory volume decrease mechanisms (RVD) (Ford et al. Biol Cell 97: 687–697, 2005). The aim of our present work was to investigate the signaling pathway that links AQP2 to this rapid RVD activation. Since it has been previously described that hypotonic conditions induce intracellular calcium ([Ca²⁺]_i) increases in different cell types, we tested the hypothesis that AQP2 could have a role in activation of calcium entry by hypotonicity and its implication in cell volume regulation. Using a fluorescent probe technique, we studied [Ca²⁺]_i and cell volume changes in response to a hypotonic shock in WT-RCCD₁ (not expressing aquaporins) and in AQP2-RCCD₁ (transfected with AQP2) cells. We found that after a hypotonic shock only AQP2-RCCD₁ cells exhibit a substantial increase in [Ca²⁺]_i. This [Ca²⁺]_i increase is strongly dependent on extracellular Ca²⁺ and is partially inhibited by thapsigargin (1 µM) indicating that the rise in [Ca²⁺]_i reflects both influx from the extracellular medium and release from intracellular stores. Exposure of AQP2-RCCD₁ cells to 100 µM gadolinium reduced the increase in [Ca²⁺]_i suggesting the involvement of a mechanosensitive calcium channel. Furthermore, exposure of cells to all of the above described conditions impaired rapid RVD. We conclude that the expression of AQP2 in the cell membrane is critical to produce the increase in [Ca²⁺]_i which is necessary to activate RVD in RCCD₁ cells.

aquaporin 2; intracellular calcium; renal cells

This article has been cited by other articles:

				U. Hasler Controlled aquaporin-2 expression in the hypertonic environment Am J Physiol Cell Physiol, April 1, 2009; 296(4): C641 - C653. [Abstract] [Full Text] [PDF]

				E. K. Hoffmann, I. H. Lambert, and S. F. Pedersen Physiology of Cell Volume Regulation in Vertebrates Physiol Rev, January 1, 2009; 89(1): 193 - 277. [Abstract] [Full Text] [PDF]