Deletion of renal Nedd4-2 abolishes the effect of high sodium intake (HS) on Kir4.1, ENaC, and NCC and causes hypokalemia during high HS-Reference-Cited by-同舟云学术

Deletion of renal Nedd4-2 abolishes the effect of high sodium intake (HS) on Kir4.1, ENaC, and NCC and causes hypokalemia during high HS

Published:2021-05-01 Issue:5 Volume:320 Page:F883-F896
ISSN:1931-857X
Container-title:American Journal of Physiology-Renal Physiology
language:en
Short-container-title:American Journal of Physiology-Renal Physiology

Author:

Zhang Dan-Dan¹²,Duan Xin-Peng²,Xiao Yu³²,Wu Peng²,Gao Zhong-Xiuzi²,Wang Wen-Hui²,Lin Dao-Hong²^ORCID

Affiliation:

1. Guangdong-Hong Kong Joint Laboratory on Immunological and Genetic Kidney Diseases, Guangdong Academy of Medical Sciences, Guangdong Provincial People’s Hospital, Guangzhou, China

2. Department of Pharmacology, New York Medical College, Valhalla, New York

3. Department of Physiology, Qiqihar Medical College, Heilongjiang, China

Abstract

The present study suggests that Nedd4-2 is involved in mediating the inhibitory effect of high salt (HS) diet on Kir4.1/kir5.1 in the distal convoluted tubule, NaCl cotransporter function, and epithelial Na+ channel activity and that Nedd4-2 plays an essential role in maintaining K+ homeostasis in response to a long-term HS diet. This suggests the possibility that HS intake could lead to hypokalemia in subjects lacking proper Nedd4-2 E3 ubiquitin ligase activity in aldosterone-sensitive distal nephron.

Funder

HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases

Publisher

American Physiological Society

Subject

Physiology

Link

https://journals.physiology.org/doi/pdf/10.1152/ajprenal.00555.2020

Reference60 articles.

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2. Immunolocalization of the ubiquitin-protein ligase Nedd4 in tissues expressing the epithelial Na+ channel (ENaC)

3. Nedd4-2 Modulates Renal Na+-Cl−Cotransporter via the Aldosterone-SGK1-Nedd4-2 Pathway