Am J Physiol Cell Physiol AJP: Gastrointestinal and Liver Physiology
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Am J Physiol Cell Physiol 293: C1187-C1208, 2007. First published August 1, 2007; doi:10.1152/ajpcell.00024.2007
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INVITED REVIEW

Functional significance of channels and transporters expressed in the inner ear and kidney

Florian Lang,1 Volker Vallon,2,3 Marlies Knipper,4 and Philine Wangemann5

1Department of Physiology, Eberhard-Karls-University of Tübingen, Tubingen, Germany; 2Departments of Medicine and Pharmacology, University of California, and 3Veterans Affairs San Diego Healthcare System, San Diego, California; 4Department of Otorhinolaryngology, Tübingen Hearing Research Centre, Molecular Neurobiology, Tübingen, Germany; and 5Department of Anatomy and Physiology, Kansas State University, Manhatten, Kansas

A number of ion channels and transporters are expressed in both the inner ear and kidney. In the inner ear, K+ cycling and endolymphatic K+, Na+, Ca2+, and pH homeostasis are critical for normal organ function. Ion channels and transporters involved in K+ cycling include K+ channels, Na+-2Cl–-K+ cotransporter, Na+/K+-ATPase, Cl– channels, connexins, and K+/Cl– cotransporters. Furthermore, endolymphatic Na+ and Ca2+ homeostasis depends on Ca2+-ATPase, Ca2+ channels, Na+ channels, and a purinergic receptor channel. Endolymphatic pH homeostasis involves H+-ATPase and Cl–/HCO3– exchangers including pendrin. Defective connexins (GJB2 and GJB6), pendrin (SLC26A4), K+ channels (KCNJ10, KCNQ1, KCNE1, and KCNMA1), Na+-2Cl–-K+ cotransporter (SLC12A2), K+/Cl– cotransporters (KCC3 and KCC4), Cl– channels (BSND and CLCNKA + CLCNKB), and H+-ATPase (ATP6V1B1 and ATPV0A4) cause hearing loss. All these channels and transporters are also expressed in the kidney and support renal tubular transport or signaling. The hearing loss may thus be paralleled by various renal phenotypes including a subtle decrease of proximal Na+-coupled transport (KCNE1/KCNQ1), impaired K+ secretion (KCNMA1), limited HCO3– elimination (SLC26A4), NaCl wasting (BSND and CLCNKB), renal tubular acidosis (ATP6V1B1, ATPV0A4, and KCC4), or impaired urinary concentration (CLCNKA). Thus, defects of channels and transporters expressed in the kidney and inner ear result in simultaneous dysfunctions of these seemingly unrelated organs.

cochlea; vestibular labyrinth; stria vascularis; deafness; renal tubule


Address for reprint requests and other correspondence: F. Lang, Dept. of Physiology, Eberhard-Karls-Univ. of Tübingen, Gmelinstrasse 5, Tübingen D-72076, Germany (e-mail: florian.lang{at}uni-tuebingen.de)




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