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Deletion of Kir5.1 abolishes the effect of high Na+ intake on Kir4.1 and Na+-Cl− cotransporter

Deletion of Kir5.1 abolishes the effect of high Na+ intake on Kir4.1 and Na+-Cl− cotransporter High-sodium-intake (HS) inhibited epithelial-sodium-channel (ENaC) in the aldosterone-sensitive-distal-nephron (ASDN) and Na+-Cl--cotransporter (NCC) by suppressing basolateral Kir4.1/Kir5.1 in the distal-convoluted-tubule (DCT) thereby increasing renal Na+ excretion but not affecting K+ excretion. The aim of the present study is to explore whether the deletion of Kir5.1 compromises the inhibitory effect of HS on NCC expression/activity and renal K+-excretion. Patch-clamp experiments demonstrated that HS failed to inhibit DCT-basolateral K+ channels and did not depolarize K+-currents (IK) reversal-potential of the DCT in Kir5.1 knockout (Kir5.1 KO) mice. Moreover, deletion of Kir5.1 not only increased the expression of Kir4.1, phosphor-NCC (pNCC) and total NCC (tNCC) but also abolished the inhibitory effect of HS on the expression of Kir4.1, pNCC and tNCC, and thiazide-induced natriuresis. Also, LS-induced stimulation of NCC expression/activity and the basolateral K+ channels in the DCT was absent in Kir5.1 KO mice. The deletion of Kir5.1 decreased ENaC currents in DCT2 and HS further inhibited ENaC activity in Kir5.1 KO mice. Finally, the measurement of basal renal K+ excretion rate with modified renal clearance method demonstrated that long-term HS inhibited renal K+ excretion rate and steadily increased plasma K+ levels in Kir5.1 KO mice but not in WT mice. We conclude that Kir5.1 plays an important role in mediating the effect of HS intake on the basolateral K+ channels in the DCT and NCC activity/expression. Kir5.1 is involved in maintaining renal ability of K+ excretion during HS intake. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png American Journal of Physiology-Renal Physiology The American Physiological Society

Deletion of Kir5.1 abolishes the effect of high Na+ intake on Kir4.1 and Na+-Cl− cotransporter

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ISSN
1931-857x
eISSN
1522-1466
DOI
10.1152/ajprenal.00004.2021
Publisher site
See Article on Publisher Site

Abstract

High-sodium-intake (HS) inhibited epithelial-sodium-channel (ENaC) in the aldosterone-sensitive-distal-nephron (ASDN) and Na+-Cl--cotransporter (NCC) by suppressing basolateral Kir4.1/Kir5.1 in the distal-convoluted-tubule (DCT) thereby increasing renal Na+ excretion but not affecting K+ excretion. The aim of the present study is to explore whether the deletion of Kir5.1 compromises the inhibitory effect of HS on NCC expression/activity and renal K+-excretion. Patch-clamp experiments demonstrated that HS failed to inhibit DCT-basolateral K+ channels and did not depolarize K+-currents (IK) reversal-potential of the DCT in Kir5.1 knockout (Kir5.1 KO) mice. Moreover, deletion of Kir5.1 not only increased the expression of Kir4.1, phosphor-NCC (pNCC) and total NCC (tNCC) but also abolished the inhibitory effect of HS on the expression of Kir4.1, pNCC and tNCC, and thiazide-induced natriuresis. Also, LS-induced stimulation of NCC expression/activity and the basolateral K+ channels in the DCT was absent in Kir5.1 KO mice. The deletion of Kir5.1 decreased ENaC currents in DCT2 and HS further inhibited ENaC activity in Kir5.1 KO mice. Finally, the measurement of basal renal K+ excretion rate with modified renal clearance method demonstrated that long-term HS inhibited renal K+ excretion rate and steadily increased plasma K+ levels in Kir5.1 KO mice but not in WT mice. We conclude that Kir5.1 plays an important role in mediating the effect of HS intake on the basolateral K+ channels in the DCT and NCC activity/expression. Kir5.1 is involved in maintaining renal ability of K+ excretion during HS intake.

Journal

American Journal of Physiology-Renal Physiology – The American Physiological Society

Published: Jun 1, 2021

References

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