Kir4.1/kir5.1 in the DCT plays a role in the regulation of renal K+ excretion

Xiao Tong Su, David H. Ellison, Wen Hui Wang

Research output: Contribution to journalReview articlepeer-review

41 Scopus citations


The aim of this mini review is to provide an overview regarding the role of inwardly rectifying potassium channel 4.1 (Kir4.1)/Kir5.1 in regulating renal K+ excretion. Deletion of Kir4.1 in the kidney inhibited thiazide-sensitive NaCl cotransporter (NCC) activity in the distal convoluted tubule (DCT) and slightly suppressed Na-K-2Cl cotransporter (NKCC2) function in the thick ascending limb (TAL). Moreover, increased dietary K+ intake inhibited, whereas decreased dietary K+ intake stimulated, the basolateral potassium channel (a Kir4.1/Kir5.1 heterote-tramer) in the DCT. The alteration of basolateral potassium conductance is essential for the effect of dietary K+ intake on NCC because deletion of Kir4.1 in the DCT abolished the effect of dietary K+ intake on NCC. Since potassium intake-mediated regulation of NCC plays a key role in regulating renal K+ excretion and potassium homeostasis, the deletion of Kir4.1 caused severe hypokalemia and metabolic alkalosis under control conditions and even during increased dietary K+ intake. Finally, recent studies have suggested that the angiotensin II type 2 receptor (AT2R) and bradykinin-B2 receptor (BK2R) are involved in mediating the effect of high dietary K+ intake on Kir4.1/Kir5.1 in the DCT.

Original languageEnglish (US)
Pages (from-to)F582-F586
JournalAmerican Journal of Physiology - Renal Physiology
Issue number3
StatePublished - Mar 2019


  • Distal convoluted tubule
  • K excretion
  • NCC
  • NKCC2

ASJC Scopus subject areas

  • Physiology
  • Urology


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