Inwardly rectifying K channels 4.1 and 5.1 (Kir4.1/Kir5.1) in the renal distal nephron

Wen Hui Wang, Dao Hong Lin

Research output: Contribution to journalReview articlepeer-review

8 Scopus citations

Abstract

The inwardly rectifying potassium channel (Kir) 4.1 (encoded by KCNJ10) interacts with Kir5.1 (encoded by KCNJ16) to form a major basolateral K channel in the renal distal convoluted tubule (DCT), connecting tubule (CNT), and the cortical collecting duct (CCD). Kir4.1/Kir5.1 heterotetramer plays an important role in regulating Na and K transport in the DCT, CNT, and CCD. A recent development in the field has firmly established the role of Kir4.1/Kir5.1 heterotetramer of the DCT in the regulation of thiazide-sensitive Na-Cl cotransporter (NCC). Changes in Kir4.1/Kir5.1 activity of the DCT are an essential step for the regulation of NCC expression/activity induced by dietary K and Na intakes and play a role in modulating NCC by type 2 angiotensin II receptor (AT2R), bradykinin type II receptor (BK2R), and β-adrenergic receptor. Since NCC activity determines the Na delivery rate to the aldosterone-sensitive distal nephron (ASDN), a distal nephron segment from late DCT to CCD, Kir4.1/Kir5.1 activity plays a critical role not only in the regulation of renal Na absorption but also in modulating renal K excretion and maintaining K homeostasis. Thus, Kir4.1/Kir5.1 activity serves as an important component of renal K sensing mechanism. The main focus of this review is to provide an overview regarding the role of Kir4.1 and Kir5.1 of the DCT and CCD in the regulation of renal Kexcretion and Na absorption.

Original languageEnglish
Pages (from-to)C277-C288
JournalAmerican Journal of Physiology - Cell Physiology
Volume323
Issue number2
DOIs
StatePublished - Aug 2022
Externally publishedYes

Keywords

  • East syndrome
  • K excretion
  • Kcnj10
  • Kcnj16
  • Na-Cl cotransporter
  • SeSAME syndrome

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