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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-52790

Wagner, C A; Capasso, G (2011). The anion exchanger pendrin (SLC26A4) and renal acid-base homeostasis. Cellular Physiology and Biochemistry, 28(3):497-504.

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Abstract

The anion exchanger pendrin (Pds, SLC26A4) transports various anions including bicarbonate, chloride and iodide. In the kidney, pendrin is exclusively expressed on the luminal pole of bicarbonate-secretory type B intercalated cells. Genetic ablation of pendrin in mice abolishes luminal chloride-bicarbonate exchanger activity from type B intercalated cells suggesting that pendrin is the apical bicarbonate extruding pathway. The renal expression of pendrin is developmentally adapted and pendrin positive cells originate from both the uretric bud and mesenchyme. In adult kidney, pendrin expression and activity is regulated by systemic acid-base status, dietary electrolyte intake (mostly chloride), and hormones such as angiotensin II and aldosterone which can affect subcellular localization, the relative number of pendrin expressing cells, and the overall abundance consistent with a role of pendrin in maintaining normal acid-base homeostasis. This review summarizes recent findings on the role and regulation of pendrin in the context of the kidneys role in acid-base homeostasis in health and disease.

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Physiology
07 Faculty of Science > Institute of Physiology

04 Faculty of Medicine > Center for Integrative Human Physiology
DDC:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2011
Deposited On:12 Dec 2011 13:41
Last Modified:28 Nov 2013 02:13
Publisher:Karger
ISSN:1015-8987
Additional Information:© 2011 S. Karger AG
Publisher DOI:10.1159/000335111
PubMed ID:22116363
Citations:Web of Science®. Times Cited: 10
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