Evidence map›Paper›PMID 22973231›Full record

ArticleFrontiers in physiology2012

βENaC is a molecular component of a VSMC mechanotransducer that contributes to renal blood flow regulation, protection from renal injury, and hypertension.

Heather A Drummond

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Epithelial NaComprehensive Physiology · 2024
    Review
  4. Article
  5. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  6. 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
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Pressure-induced constriction of the middle cerebral artery is abolished in TrpC6 knockout mice.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  13. Article
  14. 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
  15. Epithelial NaFrontiers in physiology · 2020
    Article
  16. Article
  17. Renal autoregulation in health and disease.Physiological reviews · 2015
    Review
  18. Article
  19. Inhibition of ENaC by endothelin-1.Vitamins and hormones · 2015
    Review
  20. 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.

Heather A DrummondDepartment of Physiology and Biophysics, University of Mississippi Medical Center Jackson, MS, USA.
Jackson Memorial Hospital · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI HALL, JOHN E · 1993 to 2018
$39.4M
Vascular MechanosensorR01HL086996 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI DRUMMOND, HEATHER A · 2007 to 2010
$1.4M
NHLBI NIH HHS P01 HL051971NHLBI NIH HHS R01 HL086996
6 · The paper itself

Abstract

Pressure-induced constriction (also known as the "myogenic response") is an important mechano-dependent response in certain blood vessels. The response is mediated by vascular smooth muscle cells (VSMCs) and characterized by a pressure-induced vasoconstriction in small arteries and arterioles in the cerebral, mesenteric, cardiac, and renal beds. The myogenic response has two important roles; it is a mechanism of blood flow autoregulation and provides protection against systemic blood pressure-induced damage to delicate microvessels. However, the molecular mechanism(s) underlying initiation of myogenic response is unclear. Degenerin proteins have a strong evolutionary link to mechanotransduction in the nematode. Our laboratory has addressed the hypothesis that these proteins may also act as mechanosensors in certain mammalian tissues such as VSMCs and arterial baroreceptor neurons. This article discusses the importance of a specific degenerin protein, β Epithelial Na(+) Channel (βENaC) in pressure-induced vasoconstriction in renal vessels and arterial baroreflex function as determined in a mouse model of reduced βENaC (βENaC m/m). We propose that loss of baroreflex sensitivity (due to loss of baroreceptor βENaC) increases blood pressure variability, increasing the likelihood and magnitude of upward swings in systemic pressure. Furthermore, loss of the myogenic constrictor response (due to loss of VSMC βENaC) will permit those pressure swings to be transmitted to the microvasculature in βENaC m/m mice, thus increasing the susceptibility to renal injury and hypertension.

Indexed as

baroreflexdegenerinepithelial Na+ channelhypertensionmechanotransductionmyogenic constrictionrenal blood flowrenal injury

Identifiers

PMID22973231
PMCPMC3428779
OpenAlexW2115688885

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.