Evidence map›Paper›PMID 29310825›Full record

ArticleKidney international2018

Potassium intake modulates the thiazide-sensitive sodium-chloride cotransporter (NCC) activity via the Kir4.1 potassium channel.

Ming-Xiao Wang, Catherina A Cuevas, Xiao-Tong Su, Peng Wu, Zhong-Xiuzi Gao, Dao-Hong Lin, James A McCormick, Chao-Ling Yang, Wen-Hui Wang, David H Ellison

Open access · greenAbstract read
In one paragraph

Article in Kidney international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
6.1field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

88 citing papers in PubMed, 137 citations in OpenAlex.

  1. Review
  2. Mechanistic target of rapamycin complex-1 plays a role in inhibiting kidney KAmerican journal of physiology. Renal physiology · 2026
    Article
  3. Review
  4. Article
  5. How Does Dietary Potassium Influence BP?Journal of the American Society of Nephrology : JASN · 2026
    Review
  6. Article
  7. Mechanistic target of rapamycin complex-2 mediates the effect of overnight high KAmerican journal of physiology. Renal physiology · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Angiotensin II-Type-1a Receptor and Renal K + Wasting during Overnight Low-Na + Intake.Journal of the American Society of Nephrology : JASN · 2024
    Article
  13. mTORc2 in Distal Convoluted Tubule and Renal K + Excretion during High Dietary K + Intake.Journal of the American Society of Nephrology : JASN · 2024
    Article
  14. Role of calcineurin in regulating renal potassium (KActa physiologica (Oxford, England) · 2024
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

28 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Ming-Xiao WangDepartment of Physiology, Zunyi Medical College, Zunyi, China; Department of Pharmacology, New York Medical College, Valhalla, New York, USA.
Catherina A CuevasDepartment of Medicine, Oregon Health & Science University, Portland, Oregon, USA.
Xiao-Tong SuDepartment of Pharmacology, New York Medical College, Valhalla, New York, USA.
Peng WuDepartment of Pharmacology, New York Medical College, Valhalla, New York, USA.
Zhong-Xiuzi GaoDepartment of Pharmacology, New York Medical College, Valhalla, New York, USA.
Dao-Hong LinDepartment of Pharmacology, New York Medical College, Valhalla, New York, USA.
James A McCormickDepartment of Medicine, Oregon Health & Science University, Portland, Oregon, USA.
Chao-Ling YangDepartment of Pharmacology, New York Medical College, Valhalla, New York, USA.
Wen-Hui WangDepartment of Pharmacology, New York Medical College, Valhalla, New York, USA. Electronic address: wenhui_wang@nymc.edu.
David H EllisonDepartment of Medicine, Oregon Health & Science University, Portland, Oregon, USA. Electronic address: ellisond@ohsu.edu.
New York Medical College · USOregon Health & Science University · USWestchester Medical Center · US

Funding

WNK Kinase Regulation of Thiazide-sensitive NaCl TransportR01DK051496 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI David Hoadley Ellison, CHAO-LING YANG · 1998 to 2026
$8.4M
Role of Kir4.1 in Regulating NCC and ROMK in DCTR01DK054983 · NIDDK · NEW YORK MEDICAL COLLEGE · PI ELLISON, DAVID H, WANG, WENHUI · 2001 to 2020
$7.4M
Regulation of sodium transport and blood pressure by SPAK/OSR1 kinasesR01DK098141 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI JAMES A MCCORMICK, Ujwal Shinde · 2014 to 2026
$4.2M
Role of Kir4.1 in Regulating NCC and ROMK in DCTR56DK054983 · NIDDK · NEW YORK MEDICAL COLLEGE · PI ELLISON, DAVID H, WANG, WENHUI · 2021 to 2021
$100k
Renal Effects of AldosteroneI01BX002228 · VA · PORTLAND VA MEDICAL CENTER · PI ELLISON, DAVID H · 2014 to 2021
–
BLRD VA I01 BX002228NIDDK NIH HHS R01 DK051496NIDDK NIH HHS R01 DK054983NIDDK NIH HHS R01 DK098141NIDDK NIH HHS R56 DK054983
6 · The paper itself

Abstract

Kir4.1 in the distal convoluted tubule plays a key role in sensing plasma potassium and in modulating the thiazide-sensitive sodium-chloride cotransporter (NCC). Here we tested whether dietary potassium intake modulates Kir4.1 and whether this is essential for mediating the effect of potassium diet on NCC. High potassium intake inhibited the basolateral 40 pS potassium channel (a Kir4.1/5.1 heterotetramer) in the distal convoluted tubule, decreased basolateral potassium conductance, and depolarized the distal convoluted tubule membrane in Kcnj10flox/flox mice, herein referred to as control mice. In contrast, low potassium intake activated Kir4.1, increased potassium currents, and hyperpolarized the distal convoluted tubule membrane. These effects of dietary potassium intake on the basolateral potassium conductance and membrane potential in the distal convoluted tubule were completely absent in inducible kidney-specific Kir4.1 knockout mice. Furthermore, high potassium intake decreased, whereas low potassium intake increased the abundance of NCC expression only in the control but not in kidney-specific Kir4.1 knockout mice. Renal clearance studies demonstrated that low potassium augmented, while high potassium diminished, hydrochlorothiazide-induced natriuresis in control mice. Disruption of Kir4.1 significantly increased basal urinary sodium excretion but it abolished the natriuretic effect of hydrochlorothiazide. Finally, hypokalemia and metabolic alkalosis in kidney-specific Kir4.1 knockout mice were exacerbated by potassium restriction and only partially corrected by a high-potassium diet. Thus, Kir4.1 plays an essential role in mediating the effect of dietary potassium intake on NCC activity and potassium homeostasis.

Indexed as

AlkalosisAnimalsDisease Models, AnimalFemaleHomeostasisHydrochlorothiazideHypokalemiaKcnj10 ChannelKidney Tubules, DistalKir5.1 ChannelMaleMembrane PotentialsMice, KnockoutNatriuresisPotassium Channels, Inwardly RectifyingPotassium, DietaryHydrochlorothiazideKcnj10 ChannelKir5.1 ChannelPotassium Channels, Inwardly RectifyingPotassium, DietarySlc12a3 protein, mouseSodiumSodium Chloride Symporter InhibitorsSolute Carrier Family 12, Member 3EAST syndromehyperkalemiahypokalemiaKcnj10Kcnj16

Identifiers

PMID29310825
PMCPMC6481177
OpenAlexW2781698998

What OpenQuestion holds

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Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.