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Curr Opin Nephrol Hypertens. 2008 Jan;17(1):18-24.

The interaction of pendrin and the epithelial sodium channel in blood pressure regulation.

Author information

1
Department of Medicine, Emory University School of Medicine, Atlanta, Georgia 30322, USA. smwall@emory.edu

Abstract

PURPOSE OF REVIEW:

This review summarizes the contribution of the Cl-/HCO3- exchanger pendrin in the renal regulation of blood pressure.

RECENT FINDINGS:

Intercalated cells are found in the distal convoluted tubule, the connecting tubule and the collecting duct. These cells regulate acid-base balance by secreting or absorbing OH-/H- equivalents and regulate vascular volume and blood pressure by absorbing chloride ions. In type B and non-A, non-B intercalated cells chloride absorption and HCO3- secretion are accomplished through the apical sodium-independent Cl-/HCO3- exchanger pendrin. With increased circulating aldosterone, pendrin abundance and transport are upregulated. In the absence of functional pendrin (Slc26a4 (-/-) mice), aldosterone-stimulated chloride absorption is reduced, which attenuates the blood pressure response to this steroid hormone. Pendrin also regulates aldosterone-induced changes in epithelial sodium channel abundance and function through a kidney-specific mechanism that does not involve changes in concentration of a circulating hormone. In vitro, angiotensin II increases sodium chloride absorption in the collecting duct by increasing the driving force for pendrin-mediated chloride absorption and the epithelial sodium channel-mediated sodium absorption through greater electrogenic hydrogen secretion.

SUMMARY:

Aldosterone and angiotensin II modulate the renal regulation of blood pressure, in part, by regulating pendrin-mediated chloride absorption and the epithelial sodium channel-mediated sodium absorption. Pendrin also modulates stimulation of the epithelial sodium channel by aldosterone.

PMID:
18090665
DOI:
10.1097/MNH.0b013e3282f29086
[Indexed for MEDLINE]

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