
Functional and Molecular Adaptation of Cl<sup>-</sup>/HCO<sub>3</sub><sup>-</sup> Exchanger to Chronic Alkaline Media in RenalCells
Author(s) -
Valeria Rivarola,
Paula Ford,
Osvaldo Chara,
Mario Parisi,
Claudia Capurro
Publication year - 2005
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000089853
Subject(s) - chemistry , alkalosis , homeostasis , metabolic alkalosis , intracellular ph , sodium–hydrogen antiporter , extracellular , gene isoform , ion exchange , band 3 , biophysics , ion transporter , biochemistry , endocrinology , sodium , ion , membrane , biology , gene , acidosis , membrane protein , organic chemistry
The Cl(-)/HCO3- exchanger (AE) is one of the mechanisms that cells have developed to adjust pH Despite its importance, the role of AE isoforms in controlling steady-state pH during alkalosis has not been widely investigated. In the present study, we have evaluated whether conditions simulating acute and chronic metabolic alkalosis affected the transport activity and protein levels of Cl-/HCO3- exchangers in a rat cortical collecting duct cell line (RCCD1). pH(i) was monitored using the fluorescent dye BCECF in monolayers grown on permeable supports. Anion exchanger function was assessed by the response of pH(i) to acute chloride removal. RT-PCR and immunoblot assays were also performed. Our results showed that RCCD1 cells express two members of the anion exchanger gene family: AE2 and AE4. Functional studies demonstrated that while in acute alkalosis pH(i) became alkaline and was not regulated, after 48 h adaptation; steady-state pH(i) reached a value similar to the physiological one. Chronic treated cells also resulted in a 3-fold rise in Cl(-)/HCO3- exchange activity together with a 2.2-fold increase in AE2, but not AE4, protein abundance. We conclude that RCCD1 cells can adapt to chronic extracellular alkalosis reestablishing its steady-state pH(i) and that AE2 would play a key role in cell homeostasis.