Kir4.1/Kir5.1 in the DCT plays a role in the regulation of renal K + excretion

• Published in: American journal of physiology. Renal physiology Vol. 316; no. 3; pp. F582 - F586
• Main Authors: Su, Xiao-Tong, Ellison, David H, Wang, Wen-Hui
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.03.2019
• Subjects: Animals; Biological Transport; Humans; Kidney Tubules, Distal - metabolism; Kir5.1 Channel; Potassium - metabolism; Potassium Channels, Inwardly Rectifying - metabolism; Review; Solute Carrier Family 12, Member 1 - metabolism; Solute Carrier Family 12, Member 3 - metabolism; K excretion; NKCC2; distal convoluted tubule; NCC
• ISSN: 1931-857X; 1522-1466
• DOI: 10.1152/ajprenal.00412.2018

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 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.