Regulation of Blood Pressure and Salt Balance By Pendrin-Positive Intercalated Cells: Donald Seldin Lecture 2020

• Type of Material: Article
• Authors: Susan Wall, Emory University
• Language: English
• Date: 2022-04-01
• Publisher: LIPPINCOTT WILLIAMS & WILKINS
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2022 American Heart Association, Inc.
• Final Published Version (URL): http://dx.doi.org/10.1161/HYPERTENSIONAHA.121.16492
• Title of Journal or Parent Work: HYPERTENSION
• Volume: 79
• Issue: 4
• Start Page: 706
• End Page: 716
• Grant/Funding Information: This work was supported by DK 110375 (to S.M. Wall).
• Keywords: BICARBONATE SECRETION; alkalosis; RENAL TUBULAR-ACIDOSIS; NA-CL COTRANSPORTER; Cardiovascular System & Cardiology; IMMUNOCYTOCHEMICAL LOCALIZATION; CORTICAL COLLECTING DUCT; CL-/HCO3-EXCHANGER PENDRIN; Peripheral Vascular Disease; Science & Technology; angiotensin II; H+-ATPASE; Life Sciences & Biomedicine; STIMULATES HCL SECRETION; aldosterone; blood pressure; RAT-KIDNEY; MOUSE KIDNEY; anions

Abstract

Intercalated cells make up about a third of all cells within the connecting tubule and the collecting duct and are subclassified as type A, type B and non-A, non-B based on the subcellular distribution of the H+-ATPase, which dictates whether it secretes H+or HCO3-. Type B intercalated cells mediate Cl-absorption and HCO3-secretion, which occurs largely through the anion exchanger pendrin. Pendrin is stimulated by angiotensin II via the angiotensin type 1a receptor and by aldosterone through MR (mineralocorticoid receptor). Aldosterone stimulates pendrin expression and function, in part, through the alkalosis it generates. Pendrin-mediated HCO3-secretion increases in models of metabolic alkalosis, which attenuates the alkalosis. However, pendrin-positive intercalated cells also regulate blood pressure, at least partly, through pendrin-mediated Cl-absorption and through their indirect effect on the epithelial Na+channel, ENaC. This aldosterone-induced increase in pendrin secondarily stimulates ENaC, thereby contributing to the aldosterone pressor response. This review describes the contribution of pendrin-positive intercalated cells to Na+, K+, Cl-and acid-base balance.