New perspective of CLC-KB/2 CL- channel physiology in the distal renal tubule

Oleg Zaika, Viktor Tomilin, Mykola Mamenko, Vivek Bhalla, Oleh Pochynyuk

Research output: Contribution to journalReview articlepeer-review

22 Scopus citations


Since its identification as the underlying molecular cause of Bartter's syndrome type 3, ClC-Kb (ClC-K2 in rodents, henceforth it will be referred as ClC-Kb/2) is proposed to play an important role in systemic electrolyte balance and blood pressure regulation by controlling basolateral Cl exit in the distal renal tubular segments from the cortical thick ascending limb to the outer medullary collecting duct. Considerable experimental and clinical effort has been devoted to the identification and characterization of disease-causing mutations as well as control of the channel by its cofactor, barttin. However, we have only begun to unravel the role of ClC-Kb/2 in different tubular segments and to reveal the regulators of its expression and function, e.g., insulin and IGF-1. In this review we discuss recent experimental evidence in this regard and highlight unexplored questions critical to understanding ClC-Kb/2 physiology in the kidney.

Original languageEnglish (US)
Pages (from-to)F923-F930
JournalAmerican Journal of Physiology - Renal Physiology
Issue number10
StatePublished - May 15 2016
Externally publishedYes


  • Chloride ion reabsorption
  • Collecting duct
  • Distal convoluted tuble
  • Thick ascending limb
  • pH balance

ASJC Scopus subject areas

  • Physiology
  • Urology


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