Evidence map›Paper›PMID 19553501›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2009

Pressure-induced constriction is inhibited in a mouse model of reduced betaENaC.

Lauren G VanLandingham, Kimberly P Gannon, Heather A Drummond

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

30 citing papers in PubMed, 40 citations in OpenAlex.

  1. Acid-sensing ion channel 2a assembles with epithelial NaThe Journal of biological chemistry · 2026
    Article
  2. Article
  3. Epithelial NaComprehensive Physiology · 2024
    Review
  4. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  5. Epithelial sodium channels in macrophage migration and polarization: role of proinflammatory cytokines TNFα and IFNγ.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Pressure-induced constriction of the middle cerebral artery is abolished in TrpC6 knockout mice.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  15. Article
  16. Tumor necrosis factor-α impairs cerebral blood flow in pregnant rats: role of vascular β-epithelial NaAmerican journal of physiology. Heart and circulatory physiology · 2020
    Article
  17. Article
  18. Article
  19. 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

3 authors at 1 institution in 1 country.

Lauren G VanLandinghamDept. of Physiology and Biophysics, Univ. of Mississippi Medical Center, 2500 North State St., Jackson, MS 39216-4505, USA.
Kimberly P Gannon
Heather A Drummond
University of Mississippi Medical Center · US

Funding

Vascular MechanosensorR01HL086996 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI DRUMMOND, HEATHER A · 2007 to 2010
$1.4M
NHLBI NIH HHS HL086996NHLBI NIH HHS R01 HL086996NINDS NIH HHS NS06365-01
6 · The paper itself

Abstract

Recent studies suggest certain epithelial Na(+) channel (ENaC) proteins may be components of mechanosensitive ion channel complexes in vascular smooth muscle cells that contribute to pressure-induced constriction in middle cerebral arteries (MCA). However, the role of a specific ENaC protein, betaENaC, in pressure-induced constriction of MCAs has not been determined. The goal of this study was to determine whether pressure-induced constriction in the MCA is altered in a mouse model with reduced levels of betaENaC. Using quantitative immunofluorescence, we found whole cell betaENaC labeling in cerebral vascular smooth muscle cells (VSMCs) was suppressed 46% in betaENaC homozygous mutant (m/m) mice compared with wild-type littermates (+/+). MCAs from betaENaC +/+ and m/m mice were isolated and placed in a vessel chamber for myographic analysis. Arteries from betaENaC+/+ mice constricted to stepwise increases in perfusion pressure and developed maximal tone of 10 +/- 2% at 90 mmHg (n = 5). In contrast, MCAs from betaENaC m/m mice developed significantly less tone (4 +/- 1% at 90 mmHg, n = 5). Vasoconstrictor responses to KCl (4-80 mM) were identical between genotypes and responses to phenylephrine (10(-7)-10(-4) M) were marginally altered, suggesting that reduced levels of VSMC betaENaC specifically inhibit pressure-induced constriction. Our findings indicate betaENaC is required for normal pressure-induced constriction in the MCA and provide further support for the hypothesis that betaENaC proteins are components of a mechanosensor in VSMCs.

Indexed as

Blood PressureMechanotransduction, CellularVasoconstrictionAnimalsDose-Response Relationship, DrugDown-RegulationEpithelial Sodium ChannelsMiceMice, Mutant StrainsMiddle Cerebral ArteryMuscle, Smooth, VascularMutationPhenylephrinePotassium ChlorideVasoconstrictor AgentsEpithelial Sodium ChannelsPhenylephrinePotassium ChlorideScnn1b protein, mouseVasoconstrictor Agents

Identifiers

PMID19553501
PMCPMC2739788
OpenAlexW2016065780

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.