Modus operandi of ClC-K2 Cl- Channel in the Collecting Duct Intercalated Cells

Authors

Anna Stavniichuk
Kyrylo Pyrshev
Viktor N Tomilin
Mariya Kordysh
Oleg Zaika
Oleh Pochynyuk

Publication Date

1-14-2023

Journal

Biomolecules

Abstract

The renal collecting duct is known to play a critical role in many physiological processes, including systemic water-electrolyte homeostasis, acid-base balance, and the salt sensitivity of blood pressure. ClC-K2 (ClC-Kb in humans) is a Cl--permeable channel expressed on the basolateral membrane of several segments of the renal tubule, including the collecting duct intercalated cells. ClC-Kb mutations are causative for Bartters' syndrome type 3 manifested as hypotension, urinary salt wasting, and metabolic alkalosis. However, little is known about the significance of the channel in the collecting duct with respect to the normal physiology and pathology of Bartters' syndrome. In this review, we summarize the available experimental evidence about the signaling determinants of ClC-K2 function and the regulation by systemic and local factors as well as critically discuss the recent advances in understanding the collecting-duct-specific roles of ClC-K2 in adaptations to changes in dietary Cl- intake and maintaining systemic acid-base homeostasis.

Keywords

Humans, Kidney, Bartter Syndrome, Cell Membrane, Electrolytes, Cl− intake, transcellular Cl− reabsorption, Bartters’ syndrome type 3, pendrin, AE1, acid-base transport

Comments

PMID: 36671562