Evidence map›Paper›PMID 17891415›Full record

ArticlePflugers Archiv : European journal of physiology2008

Aldosterone and amiloride alter ENaC abundance in vascular endothelium.

Kristina Kusche-Vihrog, Katja Sobczak, Nadine Bangel, Marianne Wilhelmi, Volodymyr Nechyporuk-Zloy, Albrecht Schwab, Hermann Schillers, Hans Oberleithner

Abstract read
PubMed Publisher
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

53 citing papers in PubMed, 110 citations in OpenAlex.

  1. ENAC blockade reduces blood pressure and arterial stiffness in adults with obesity and insulin resistance.American journal of physiology. Heart and circulatory physiology · 2026
    Trial
  2. Review
  3. SECS, drugs, and Rac1&Rho: regulation of EnNaC in vascular endothelial cells.Pflugers Archiv : European journal of physiology · 2025
    Article
  4. Article
  5. Review
  6. Epithelial NaComprehensive Physiology · 2024
    Review
  7. Article
  8. Article
  9. Salt Sensitivity of Blood Pressure in Women.Hypertension (Dallas, Tex. : 1979) · 2023
    Review
  10. Mineralocorticoid receptor-antagonism prevents COVID-19-dependent glycocalyx damage.Pflugers Archiv : European journal of physiology · 2022
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Epithelial Sodium Channel and Salt-Sensitive Hypertension.Hypertension (Dallas, Tex. : 1979) · 2021
    Review
  16. Review
  17. Review
  18. Epithelial NaFrontiers in physiology · 2020
    Article
  19. Endothelial Dysfunction in Primary Aldosteronism.International journal of molecular sciences · 2019
    Review
  20. Article
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

8 authors at 1 institution in 1 country.

Kristina Kusche-VihrogInstitute of Animal Physiology, University of Muenster, Hindenburgplatz 55, 48143 Muenster, Germany. kusche@uni-muenster.de
Katja Sobczak
Nadine Bangel
Marianne Wilhelmi
Volodymyr Nechyporuk-Zloy
Albrecht Schwab
Hermann Schillers
Hans Oberleithner
University of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The amiloride-sensitive epithelial sodium channel (ENaC) is usually found in the apical membrane of epithelial cells but has also recently been described in vascular endothelium. Because little is known about the regulation and cell surface density of ENaC, we studied the influence of aldosterone, spironolactone, and amiloride on its abundance in the plasma membrane of human endothelial cells. Three different methods were applied, single ENaC molecule detection in the plasma membrane, quantification by Western blotting, and cell surface imaging using atomic force microscopy. We found that aldosterone increases the surface expression of ENaC molecules by 36% and the total cellular amount by 91%. The aldosterone receptor antagonist spironolactone prevents these effects completely. Acute application of amiloride to aldosterone-pretreated cells led to a decline of intracellular ENaC by 84%. We conclude that, in vascular endothelium, aldosterone induces ENaC expression and insertion into the plasma membrane. Upon functional blocking with amiloride, the channel disappears from the cell surface and from intracellular pools, indicating either rapid degradation and/or membrane pinch-off. This opens new perspectives in the regulation of ENaC expressed in the vascular endothelium.

Indexed as

AldosteroneAmilorideBlotting, WesternCell MembraneCell Membrane PermeabilityCells, CulturedDiureticsEndothelial CellsEpithelial Sodium ChannelsFluorescent Antibody TechniqueHumansMicroscopy, Atomic ForceSpironolactoneUmbilical VeinsAldosteroneAmilorideDiureticsEpithelial Sodium ChannelsSpironolactone

Identifiers

PMID17891415
OpenAlexW2129762317

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.