Evidence map›Paper›PMID 19889952›Full record

ArticleAmerican journal of physiology. Renal physiology2010

Altered whole kidney blood flow autoregulation in a mouse model of reduced beta-ENaC.

Samira C Grifoni, Rumbidzayi Chiposi, Susan E McKey, Michael J Ryan, Heather A Drummond

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 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

35 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Epithelial NaComprehensive Physiology · 2024
    Review
  5. Article
  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. Article
  8. Renal blood flow and oxygenation.Pflugers Archiv : European journal of physiology · 2022
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  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. Epithelial NaAnnual review of physiology · 2018
    Review
  19. 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

5 authors at 1 institution in 1 country.

Samira C GrifoniDepartment of Physiology and Biophysics and the Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi 39216-4505, USA.
Rumbidzayi Chiposi
Susan E McKey
Michael J Ryan
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 HL-086996NHLBI NIH HHS R01 HL086996
6 · The paper itself

Abstract

Renal blood flow (RBF) autoregulation is mediated by at least two mechanisms, the fast acting myogenic response (approximately 5 s) and slow acting tubuloglomerular feedback (TGF; approximately 25 s). Previous studies suggest epithelial Na(+) channel (ENaC) family proteins, beta-ENaC in particular, mediate myogenic constriction in isolated renal interlobar arteries. However, it is unknown whether beta-ENaC-mediated myogenic constriction contributes to RBF autoregulation in vivo. Therefore, the goal of this investigation was to determine whether the myogenic mediated RBF autoregulation is inhibited in a mouse model of reduced beta-ENaC (m/m). To address this goal, we evaluated the temporal response of RBF and renal vascular resistance (RVR) to a 2-min step increase in mean arterial pressure (MAP). Pressure-induced changes in RBF and RVR at 0-5, 6-25, and 110-120 s after step increase in MAP were used to assess the contribution of myogenic and TGF mechanisms and steady-state autoregulation, respectively. The rate of the initial increase in RVR, attributed to the myogenic mechanism, was reduced by approximately 50% in m/m mice, indicating the speed of the myogenic response was inhibited. Steady-state autoregulation was similar between beta-ENaC +/+ and m/m mice. Although the rate of the secondary increase in RVR, attributed to TGF, was similar in beta-ENaC +/+ and m/m mice, however, it occurred over a longer period (+10 s), which may have allowed TGF to compensate for a loss in myogenic autoregulation. Our findings suggest beta-ENaC is an important mediator of renal myogenic constriction-mediated RBF autoregulation in vivo.

Indexed as

HomeostasisAdaptation, PhysiologicalAnimalsBlood PressureDown-RegulationEpithelial Sodium ChannelsFeedback, PhysiologicalHemodynamicsKidney GlomerulusKidney TubulesMiceMice, Mutant StrainsMuscle, Smooth, VascularRenal CirculationTime FactorsVascular ResistanceEpithelial Sodium Channels

Identifiers

PMID19889952
PMCPMC2822522
OpenAlexW1985386277

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.