Evidence map›Paper›PMID 20383718›Full record

ReviewPflugers Archiv : European journal of physiology2010

Endothelium-derived hyperpolarising factors and associated pathways: a synopsis.

Gillian Edwards, Michel Félétou, Arthur H Weston

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers.

0numbers the graph read from it
0cells of the map it votes in
168citing papers in PubMed
20.0field-weighted citation impact, top 1% 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

168 citing papers in PubMed, 356 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Bilobalide increases SKBMC complementary medicine and therapies · 2026
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  8. Review
  9. Review
  10. Perivascular Adipose Tissue and Uterine Artery Adaptations to Pregnancy.Microcirculation (New York, N.Y. : 1994) · 2024
    Review
  11. Review
  12. WNK kinase is a vasoactive chloride sensor in endothelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. Review
  14. Sitting leg vasculopathy: potential adaptations beyond the endothelium.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Pharmaceutical biology · 2022
    Article
  20. Article

108 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Gillian EdwardsFaculty of Life Sciences, University of Manchester, CTF Building, 46 Grafton St, Manchester, M13 9NT, UK.
Michel Félétou
Arthur H Weston
University of Manchester · GBServier (France) · FR

Funding

British Heart Foundation
6 · The paper itself

Abstract

The term endothelium-derived hyperpolarising factor (EDHF) was introduced in 1987 to describe the hypothetical factor responsible for myocyte hyperpolarisations not associated with nitric oxide (EDRF) or prostacyclin. Two broad categories of EDHF response exist. The classical EDHF pathway is blocked by apamin plus TRAM-34 but not by apamin plus iberiotoxin and is associated with endothelial cell hyperpolarisation. This follows an increase in intracellular [Ca(2+)] and the opening of endothelial SK(Ca) and IK(Ca) channels preferentially located in caveolae and in endothelial cell projections through the internal elastic lamina, respectively. In some vessels, endothelial hyperpolarisations are transmitted to myocytes through myoendothelial gap junctions without involving any EDHF. In others, the K(+) that effluxes through SK(Ca) activates myocytic and endothelial Ba(2+)-sensitive K(IR) channels leading to myocyte hyperpolarisation. K(+) effluxing through IK(Ca) activates ouabain-sensitive Na(+)/K(+)-ATPases generating further myocyte hyperpolarisation. For the classical pathway, the hyperpolarising "factor" involved is the K(+) that effluxes through endothelial K(Ca) channels. During vessel contraction, K(+) efflux through activated myocyte BK(Ca) channels generates intravascular K(+) clouds. These compromise activation of Na(+)/K(+)-ATPases and K(IR) channels by endothelium-derived K(+) and increase the importance of gap junctional electrical coupling in myocyte hyperpolarisations. The second category of EDHF pathway does not require endothelial hyperpolarisation. It involves the endothelial release of factors that include NO, HNO, H(2)O(2) and vasoactive peptides as well as prostacyclin and epoxyeicosatrienoic acids. These hyperpolarise myocytes by opening various populations of myocyte potassium channels, but predominantly BK(Ca) and/or K(ATP), which are sensitive to blockade by iberiotoxin or glibenclamide, respectively.

Indexed as

AnimalsApaminBiological FactorsCarbon MonoxideEicosanoidsEndothelium-Dependent Relaxing FactorsEndothelium, VascularEpoprostenolHumansHydrogen PeroxideMuscle CellsNatriuretic Peptide, C-TypeNitric OxidePotassiumPotassium Channel BlockersPotassium ChannelsApaminBiological FactorsCarbon MonoxideEicosanoidsendothelium-dependent hyperpolarization factorEndothelium-Dependent Relaxing FactorsEpoprostenolHydrogen PeroxideNatriuretic Peptide, C-TypeNitric OxidePotassiumPotassium Channel BlockersPotassium ChannelsPotassium Channels, Calcium-ActivatedPyrazolesSmall-Conductance Calcium-Activated Potassium ChannelsSodium-Potassium-Exchanging ATPaseTRAM 34

Identifiers

PMID20383718
OpenAlexW1982580263

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.