Kidney Res Clin Pract.
2017 Dec;36(4):305-317. 10.23876/j.krcp.2017.36.4.305.
Renal intercalated cells and blood pressure regulation
- Affiliations
-
- 1Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA. smwall@emory.edu
- 2Department of Physiology, Emory University School of Medicine, Atlanta, GA, USA.
- KMID: 2405106
- DOI: http://doi.org/10.23876/j.krcp.2017.36.4.305
Abstract
- 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 Clâ» absorption and HCO₃⻠secretion largely through pendrin-dependent Clâ»/HCO₃⻠exchange. This exchange is stimulated by angiotensin II administration and is also stimulated in models of metabolic alkalosis, for instance after aldosterone or NaHCO₃ administration. In some rodent models, pendrin-mediated HCO₃⻠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 Clâ» absorption, but also by modulating the aldosterone response for epithelial Na⺠channel (ENaC)-mediated Na⺠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.
