Evidence map›Paper›PMID 20702602›Full record

ArticleAmerican journal of physiology. Renal physiology2010

Effects of dietary K on cell-surface expression of renal ion channels and transporters.

Gustavo Frindt, Lawrence G Palmer

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

86 citing papers in PubMed, 123 citations in OpenAlex.

  1. Why Your Mother Was Right: How Potassium Intake Reduces Blood Pressure.Transactions of the American Clinical and Climatological Association · 2015
    Trial
  2. Mechanistic target of rapamycin complex-1 plays a role in inhibiting kidney KAmerican journal of physiology. Renal physiology · 2026
    Article
  3. ENaC processing in rat kidney: effects of salt loading and ADH.American journal of physiology. Renal physiology · 2026
    Article
  4. Potassium and the kidney.Nature reviews. Nephrology · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. High dietary KAmerican journal of physiology. Renal physiology · 2023
    Article
  17. Article
  18. Renal KFrontiers in physiology · 2023
    Review
  19. Directing two-way traffic in the kidney: A tale of two ions.The Journal of general physiology · 2022
    Article
  20. Potassium homeostasis: sensors, mediators, and targets.Pflugers Archiv : European journal of physiology · 2022
    Review

26 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

2 authors at 1 institution in 1 country.

Gustavo FrindtDept. Physiology and Biophysics, Weill Medical College of Cornell Univ., 1300 York Ave., New York, NY 10065, USA.
Lawrence G Palmer
Cornell University · US

Funding

Molecular of ROMK Channel FunctionR01DK054231 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI Paul A Welling · 1998 to 2026
$7.7M
MEMBRANE PROCESSES MEDIATING NACL TRANSPORTR01DK027847 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI PALMER, LAWRENCE G · 1986 to 2013
$4.8M
Epithelial Na Channels and Regulation of Na ExcretionR01DK059659 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI PALMER, LAWRENCE G · 2002 to 2012
$3.7M
NIDDK NIH HHS DK27847NIDDK NIH HHS DK54231NIDDK NIH HHS DK59659NIDDK NIH HHS R01 DK027847NIDDK NIH HHS R01 DK059659
6 · The paper itself

Abstract

Changes in apical surface expression of ion channels and transporters in the superficial rat renal cortex were assessed using biotinylation and immunoblotting during alterations in dietary K intake. A high-K diet increased, and a low-K diet decreased, both the overall and surface abundance of the β- and γ-subunits of the epithelial Na channel (ENaC). In the case of γ-ENaC, the effect was specific for the 65-kDa cleaved form of the protein. The overall amount of α-ENAC was also increased with increasing K intake. The total expression of the secretory K(+) channels (ROMK) increased with a high-K diet and decreased with a low-K diet. The surface expression of ROMK increased with high K intake but was not significantly altered by a low-K diet. In contrast, the amounts of total and surface protein representing the thiazide-sensitive NaCl cotransporter (NCC) decreased with increasing K intake. We conclude that modulation of K(+) secretion in response to changes in dietary K intake involves changes in apical K(+) permeability through regulation of K(+) channels and in driving force subsequent to alterations in both Na delivery to the distal nephron and Na(+) uptake across the apical membrane of the K(+) secretory cells.

Indexed as

AnimalsEpithelial Sodium ChannelsFemaleKidney CortexMaleModels, AnimalNephronsOocytesPotassium ChannelsPotassium Channels, Inwardly RectifyingPotassium, DietaryRatsRats, Sprague-DawleySodiumSodium Chloride SymportersXenopus laevisEpithelial Sodium ChannelsKcnj1 protein, ratPotassium ChannelsPotassium Channels, Inwardly RectifyingPotassium, DietarySodiumSodium Chloride Symporters

Identifiers

PMID20702602
PMCPMC2957263
OpenAlexW2137895593

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.