| Volume regulation in cortical collecting duct cells: role of AQP2. | |
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MedLine Citation:
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PMID: 15859948 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND INFORMATION: The renal CCD (cortical collecting duct) plays a role in final volume and concentration of urine by a process that is regulated by the antidiuretic hormone, [arginine]vasopressin. This hormone induces an increase in water permeability due to the translocation of AQP2 (aquaporin 2) from the intracellular vesicles to the apical membrane of principal cells. During the transition from antidiuresis to diuresis, CCD cells are exposed to changes in environmental osmolality, and cell-volume regulation may be especially important for the maintenance of intracellular homoeostasis. Despite its importance, cell-volume regulation in CCD cells has not been widely investigated. Moreover, no studies have been carried out till date to evaluate the putative role of AQPs during this process in renal cells. RESULTS: In the present study, we have studied the regulatory cell-volume responses to hypo-osmotic or hyperosmotic challenges in two CCD cell lines: one not expressing AQPs and the other stably transfected with AQP2. We have used a fluorescent probe technique in which the acquisition of single-cell kinetic data can be simultaneously recorded with the intracellular pH. Experiments with hyperosmotic mannitol media demonstrated that, independent of AQP2 expression, CCD cells shrink but fail to show regulatory volume increase, at least under the studied conditions. In contrast, under hypo-osmotic shocks, regulatory volume decrease occurs and the activation of these mechanisms is more rapid in AQP2 transfected cells. This regulatory response takes place in parallel with intracellular acidification, which is faster in cells expressing AQP2. The acidification and the initial regulatory volume decrease response were inhibited by glibenclamide and BaCl2 only in AQP2 cells. CONCLUSIONS: These results suggest that increases in the osmotic water permeability due to the expression of AQP2 are critical for a rapid activation of regulatory volume decrease mechanisms, which would be linked to cystic fibrosis transmembrane conductance regulator and to barium-sensitive potassium channels. |
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Authors:
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Paula Ford; Valeria Rivarola; Osvaldo Chara; Marcel Blot-Chabaud; Françoise Cluzeaud; Nicolette Farman; Mario Parisi; Claudia Capurro |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Biology of the cell / under the auspices of the European Cell Biology Organization Volume: 97 ISSN: 0248-4900 ISO Abbreviation: Biol. Cell Publication Date: 2005 Sep |
Date Detail:
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Created Date: 2005-08-17 Completed Date: 2005-11-04 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8108529 Medline TA: Biol Cell Country: England |
Other Details:
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Languages: eng Pagination: 687-97 Citation Subset: IM |
Affiliation:
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Laboratorio de Biomembranas, Departamento de Fisiología y Biofísica, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, piso 7, 1121 Buenos Aires, Argentina. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Anti-Arrhythmia Agents / metabolism Aquaporin 2 Aquaporins / metabolism* Barium Compounds / metabolism Cell Line Cell Membrane Permeability* Cell Size* Chlorides / metabolism Glyburide / metabolism Hydrogen-Ion Concentration Kidney Tubules, Collecting / cytology*, metabolism* Mannitol / metabolism Osmolar Concentration Rats Urea / metabolism Water / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Anti-Arrhythmia Agents; 0/Aqp2 protein, rat; 0/Aquaporin 2; 0/Aquaporins; 0/Barium Compounds; 0/Chlorides; 10238-21-8/Glyburide; 10361-37-2/barium chloride; 57-13-6/Urea; 69-65-8/Mannitol; 7732-18-5/Water |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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