Evidence map›Paper›PMID 22471931›Full record

ReviewAnnals of medicine2012

Two barriers for sodium in vascular endothelium?

Hans Oberleithner

Open access · bronzeAbstract readReview
In one paragraph

Review in Annals of medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Effects of excess sodium consumption on arterial function in C57BL/6 mice.American journal of physiology. Heart and circulatory physiology · 2024
    Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Current Understanding of Pressure Natriuresis.Electrolyte & blood pressure : E & BP · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Role of the vascular wall in sodium homeostasis and salt sensitivity.Journal of the American Society of Nephrology : JASN · 2015
    Review
  19. Salt controls endothelial and vascular phenotype.Pflugers Archiv : European journal of physiology · 2015
    Review
  20. Salt and gene expression: evidence for [Na+]i/[K+]i-mediated signaling pathways.Pflugers Archiv : European journal of physiology · 2015
    Review
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

1 author at 1 institution in 1 country.

Hans OberleithnerInstitute of Physiology II, University of Münster, Münster, Germany. oberlei@uni-muenster.de
University of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular endothelium plays a key role in blood pressure regulation. Recently, it has been shown that a 5% increase of plasma sodium concentration (sodium excess) stiffens endothelial cells by about 25%, leading to cellular dysfunction. Surface measurements demonstrated that the endothelial glycocalyx (eGC), an anionic biopolymer, deteriorates when sodium is elevated. In view of these results, a two-barrier model for sodium exiting the circulation across the endothelium is suggested. The first sodium barrier is the eGC which selectively buffers sodium ions with its negatively charged proteoglycans. The second sodium barrier is the endothelial plasma membrane which contains sodium channels. Sodium excess, in the presence of aldosterone, leads to eGC break-down and, in parallel, to an up-regulation of plasma membrane sodium channels. The following hypothesis is postulated: Sodium excess increases vascular sodium permeability. Under such conditions (e.g. high-sodium diet), day-by-day ingested sodium, instead of being readily buffered by the eGC and then rapidly excreted by the kidneys, is distributed in the whole body before being finally excreted. Gradually, the sodium overload damages the organism.

Indexed as

Blood PressureEndothelium, VascularGlycocalyxHomeostasisHumansPermeabilitySodiumSodium ChannelsSodiumSodium Channels

Identifiers

PMID22471931
PMCPMC3470790
OpenAlexW2021676874

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.