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Author Notes:

Correspondence to: Susan M. Wall, Renal Division, Departments of Medicine and Physiology, Emory University School of Medicine, WMB Rm. 338, 1639 Pierce Dr., NE, Atlanta, GA 30322, USA. E-mail: smwall@emory.edu.

I thank Dr. Peter Kopp for his suggestions.

The author has no conflicts of interest to declare.


Research Funding:

This work was supported by NIH grant DK 104125 (to S. M. Wall).


  • Blood pressure
  • Cl−/HCO3− exchange
  • Epithelial sodium channels
  • Intercalated cells
  • Pendrin
  • Slc26a4

Renal intercalated cells and blood pressure regulation


Journal Title:

Kidney Research and Clinical Practice


Volume 36, Number 4


, Pages 305-317

Type of Work:

Article | Final Publisher PDF


Type B and non-A, non-B intercalated cells are found within the connecting tubule and the cortical collecting duct. Of these cell types, type B intercalated cells are known to mediate Cl - absorption and HCO 3 - secretion largely through pendrin-dependent Cl - /HCO 3 - exchange. This exchange is stimulated by angiotensin II administration and is also stimulated in models of metabolic alkalosis, for instance after aldosterone or NaHCO 3 administration. In some rodent models, pendrin-mediated HCO 3 - secretion modulates acid-base balance. However, the role of pendrin in blood pressure regulation is likely of more physiological or clinical significance. Pendrin regulates blood pressure not only by mediating aldosterone-sensitive Cl - absorption, but also by modulating the aldosterone response for epithelial Na + channel (ENaC)-mediated Na + absorption. Pendrin regulates ENaC through changes in open channel of probability, channel surface density, and channels subunit total protein abundance. Thus, aldosterone stimulates ENaC activity through both direct and indirect effects, the latter occurring through its stimulation of pendrin expression and function. Therefore, pendrin contributes to the aldosterone pressor response. Pendrin may also modulate blood pressure in part through its action in the adrenal medulla, where it modulates the release of catecholamines, or through an indirect effect on vascular contractile force. This review describes how aldosterone and angiotensin II-induced signaling regulate pendrin and the contributory role of pendrin in distal nephron function and blood pressure.

Copyright information:

© 2017 by The Korean Society of Nephrology.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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