The Cl−/HCO3−exchanger pendrin in the rat kidney is regulated in response to chronic alterations in chloride balance

Quentin, Fabienne; Chambrey, Régine; Trinh–Trang–Tan, Marie–Marcelle; Fysekidis, Marinos; Cambillau, Michèle; Paillard, Michel; Aronson, Peter S.; Eladari, Dominique

doi:10.1152/ajprenal.00211.2004

Cited by 113 publications

(116 citation statements)

References 43 publications

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“…Pendrin is upregulated by the injection of deoxycorticosterone pivalate, a pharmacologic analogue of aldosterone (16). However, we have demonstrated that pendrin also can be regulated in response to changes in Cl Ϫ intake by an aldosterone-independent mechanism (17). In vivo relevance of both mechanisms remains unsettled, but this question is of particular importance.…”

Section: CLmentioning

confidence: 89%

“…Membrane fraction preparation and immunoblotting procedures for comparing two sets of samples of renal cortical membranes with regard to relative abundance of specific proteins were described in detail previously (17,24). Coomassie blue-stained polyacrylamide gels were used to control equality of protein loading for each series, as described in detail previously (17,24).…”

Section: Immunoblot Analysesmentioning

confidence: 99%

“…Coomassie blue-stained polyacrylamide gels were used to control equality of protein loading for each series, as described in detail previously (17,24). The dilutions of primary antibodies used in this study were as follows: Anti-pendrin, 1:30,000; anti-H ϩ -ATPase, 1:30,000; anti-␣-ENaC, 1:3000; anti-␤-ENaC, 1:20,000; and anti-␥-ENaC, 1:2000.…”

Section: Immunoblot Analysesmentioning

confidence: 99%

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Pendrin Regulation in Mouse Kidney Primarily Is Chloride-Dependent

Vallet

Picard²,

Loffing‐Cueni³

et al. 2006

Journal of the American Society of Nephrology

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Recent studies indicate that pendrin, an apical Cl ؊ /HCO 3 ؊ exchanger, mediates chloride reabsorption in the connecting tubule and the cortical collecting duct and therefore is involved in extracellular fluid volume regulation. The purpose of this study was to test whether pendrin is regulated in vivo primarily by factors that are associated with changes in renal chloride transport, by aldosterone, or by the combination of both determinants. For achievement of this goal, pendrin protein abundance was studied by semiquantitative immunoblotting in different mouse models with altered aldosterone secretion or tubular chloride transport, including NaCl loading, hydrochlorothiazide administration, NaCl co-transporter knockout mice, and mice with Liddle's mutation. The parallel regulation of the aldosterone-regulated epithelial sodium channel (ENaC) was examined as a control for biologic effects of aldosterone. Major changes in pendrin protein expression were found in experimental models that are associated with altered renal chloride transport, whereas no significant changes were detected in pendrin protein abundance in models with altered aldosterone secretion. Moreover, in response to hydrochlorothiazide administration, pendrin was downregulated despite a marked secondary hyperaldosteronism. In contrast, ␣-ENaC was markedly upregulated, and the molecular weight of a large fraction of ␥-ENaC subunits was shifted from 85 to 70 kD, consistent with previous results from rat models with elevated plasma aldosterone levels. These results suggest that factors that are associated with changes in distal chloride delivery govern pendrin expression in the connecting tubule and cortical collecting duct.

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Section: CLmentioning

confidence: 89%

Section: Immunoblot Analysesmentioning

confidence: 99%

Section: Immunoblot Analysesmentioning

confidence: 99%

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Pendrin Regulation in Mouse Kidney Primarily Is Chloride-Dependent

Vallet

Picard²,

Loffing‐Cueni³

et al. 2006

Journal of the American Society of Nephrology

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“…Increased chloride delivery to the distal nephron and collecting duct is associated with reduced pendrin expression levels (139,192). Apparently, pendrin expression is sensitive to luminal chloride concentration but less to systemic chloride status.…”

Section: Ae1mentioning

confidence: 99%

“…A role of pendrin in collecting duct chloride reabsorption is further supported by the findings that pendrin expression is regulated during chloride depletion (197,208), Pds KO mice are resistant to DOCA and NaCl induced hypertension (196), and angiotensin II stimulates chloride reabsorption in isolated CCDs from wildtype but not from pendrin deficient mice (132) Pendrin activity may be controlled on at least four different levels, namely mRNA and protein expression as well as subcellular localization. Enhanced luminal pendrin localization was observed in animals loaded with bicarbonate (203), given DOCA (196), or during chloride depletion (197), whereas several treatments altered total pendrin abundance in the kidney (57,67,139,192,203). Studies in various cell lines provided evidence for direct regulatory domains in the promoter region sensitive to intracellular pH and possibly to aldosterone (1).…”

Section: Ae1mentioning

confidence: 99%

Regulated acid–base transport in the collecting duct

Wagner

Devuyst

Bourgeois

et al. 2009

Pflugers Arch - Eur J Physiol

161

142

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The renal collecting system serves the fine-tuning of renal acid-base secretion. Acid-secretory type-A intercalated cells secrete protons via a luminally expressed V-type H(+)-ATPase and generate new bicarbonate released by basolateral chloride/bicarbonate exchangers including the AE1 anion exchanger. Efficient proton secretion depends both on the presence of titratable acids (mainly phosphate) and the concomitant secretion of ammonia being titrated to ammonium. Collecting duct ammonium excretion requires the Rhesus protein RhCG as indicated by recent KO studies. Urinary acid secretion by type-A intercalated cells is strongly regulated by various factors among them acid-base status, angiotensin II and aldosterone, and the Calcium-sensing receptor. Moreover, urinary acidification by H(+)-ATPases is modulated indirectly by the activity of the epithelial sodium channel ENaC. Bicarbonate secretion is achieved by non-type-A intercalated cells characterized by the luminal expression of the chloride/bicarbonate exchanger pendrin. Pendrin activity is driven by H(+)-ATPases and may serve both bicarbonate excretion and chloride reabsorption. The activity and expression of pendrin is regulated by different factors including acid-base status, chloride delivery, and angiotensin II and may play a role in NaCl retention and blood pressure regulation. Finally, the relative abundance of type-A and non-type-A intercalated cells may be tightly regulated. Dysregulation of intercalated cell function or abundance causes various syndromes of distal renal tubular acidosis underlining the importance of these processes for acid-base homeostasis.

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Uriniferous Tubule: Structural and Functional Organization

Christensen

Wagner

Kaissling

2012

Comprehensive Physiology

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The uriniferous tubule is divided into the proximal tubule, the intermediate (thin) tubule, the distal tubule and the collecting duct. The present chapter is based on the chapters by Maunsbach and Christensen on the proximal tubule, and by Kaissling and Kriz on the distal tubule and collecting duct in the 1992 edition of the Handbook of Physiology, Renal Physiology. It describes the fine structure (light and electron microscopy) of the entire mammalian uriniferous tubule, mainly in rats, mice, and rabbits. The structural data are complemented by recent data on the location of the major transport‐ and transport‐regulating proteins, revealed by morphological means (immunohistochemistry, immunofluorescence, and/or mRNA in situ hybridization). The structural differences along the uriniferous tubule strictly coincide with the distribution of the major luminal and basolateral transport proteins and receptors and both together provide the basis for the subdivision of the uriniferous tubule into functional subunits. Data on structural adaptation to defined functional changes in vivo and to genetical alterations of specified proteins involved in transepithelial transport importantly deepen our comprehension of the correlation of structure and function in the kidney, of the role of each segment or cell type in the overall renal function, and our understanding of renal pathophysiology. © 2012 American Physiological Society. Compr Physiol 2:805‐861, 2012.

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The Cl⁻/HCO₃⁻exchanger pendrin in the rat kidney is regulated in response to chronic alterations in chloride balance

Cited by 113 publications

References 43 publications

Pendrin Regulation in Mouse Kidney Primarily Is Chloride-Dependent

Pendrin Regulation in Mouse Kidney Primarily Is Chloride-Dependent

Regulated acid–base transport in the collecting duct

Uriniferous Tubule: Structural and Functional Organization

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