NYMC Faculty Publications


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

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January 2019




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.