PDF(Pubmed)
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 K+ excretion and Na+ absorption.
摘要：
向内整流钾通道（Kir）4.1（由KCNJ10编码）与Kir5.1（由KCNJ16编码）相互作用，在肾远曲小管（DCT）中形成主要的基底外侧K通道，连接管（CNT），和皮质集合管（CCD）。Kir4.1/Kir5.1异四聚体在DCT中调节Na+和K+转运中起重要作用，CNT,和CCD。该领域的最新发展已牢固地确立了DCT的Kir4.1/Kir5.1异四聚体在调节噻嗪敏感的Na-Cl协同转运蛋白（NCC）中的作用。DCT的Kir4.1/Kir5.1活性的变化是调节饮食K和Na摄入诱导的NCC表达/活性的重要步骤，并在通过2型血管紧张素II受体（AT2R）调节NCC中发挥作用，缓激肽II型受体（BK2R），和β-肾上腺素能受体。由于NCC活性决定了醛固酮敏感性远端肾单位（ASDN）的Na+递送率，从晚期DCT到CCD的远端肾单位段，Kir4.1/Kir5.1活性不仅在调节肾脏Na吸收中起关键作用，而且在调节肾脏K排泄和维持K稳态中起关键作用。因此，Kir4.1/Kir5.1活性是肾脏K+传感机制的重要组成部分。这篇综述的主要重点是概述DCT和CCD的Kir4.1和Kir5.1在调节肾脏K排泄和Na吸收中的作用。
