NYMC Faculty Publications

Kir4.1/5.1 in the DCT Plays a Role in the Regulation of Renal K+ Excretion

DOI

10.1152/ajprenal.00412.2018

Journal Title

American Journal of Physiology.Renal Physiology

First Page

F582

Last Page

F586

Document Type

Article

Publication Date

January 2019

Department

Pharmacology

Abstract

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 heterotetramer) in the DCT. The alteration of the 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 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.

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