Evidence map›Paper›PMID 26541094›Full record

ReviewMicrocirculation (New York, N.Y. : 1994)2016

Endothelium-Derived Hyperpolarization and Coronary Vasodilation: Diverse and Integrated Roles of Epoxyeicosatrienoic Acids, Hydrogen Peroxide, and Gap Junctions.

David C Ellinsworth, Shaun L Sandow, Nilima Shukla, Yanping Liu, Jamie Y Jeremy, David D Gutterman

Abstract readReview
In one paragraph

Review in Microcirculation (New York, N.Y. : 1994), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 61 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Reactive Oxygen Species and Endothelial CaInternational journal of molecular sciences · 2021
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Protection from vascular dysfunction in female rats with chronic stress and depressive symptoms.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  19. Article
  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

6 authors at 5 institutions in 3 countries.

David C EllinsworthBristol Heart Institute, University of Bristol, Bristol, UK.
Shaun L SandowFaculty of Science, Health, Education and Engineering, University of the Sunshine Coast, Maroochydore, Queensland, Australia.
Nilima ShuklaBristol Heart Institute, University of Bristol, Bristol, UK.
Yanping LiuDivision of Research Infrastructure, National Center for Research Resources, National Institutes of Health, Bethesda, Maryland, USA.
Jamie Y JeremyBristol Heart Institute, University of Bristol, Bristol, UK.
David D GuttermanDivision of Cardiovascular Medicine, Departments of Medicine, Physiology and Pharmacology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
University of Bristol · GBMedical College of Wisconsin · USNational Institutes of Health · USNIHR Bristol Cardiovascular Biomedical Research Unit · GBUniversity of the Sunshine Coast · AU

Funding

Mechanism of Flow-Induced Dilation in the Human MicrocirculationR01HL113612 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GUTTERMAN, DAVID D. · 2013 to 2016
$1.7M
NHLBI NIH HHS HL113612NHLBI NIH HHS R01 HL113612
6 · The paper itself

Abstract

Myocardial perfusion and coronary vascular resistance are regulated by signaling metabolites released from the local myocardium that act either directly on the VSMC or indirectly via stimulation of the endothelium. A prominent mechanism of vasodilation is EDH of the arteriolar smooth muscle, with EETs and H(2)O(2) playing important roles in EDH in the coronary microcirculation. In some cases, EETs and H(2)O(2) are released as transferable hyperpolarizing factors (EDHFs) that act directly on the VSMCs. By contrast, EETs and H(2)O(2) can also promote endothelial KCa activity secondary to the amplification of extracellular Ca(2+) influx and Ca(2+) mobilization from intracellular stores, respectively. The resulting endothelial hyperpolarization may subsequently conduct to the media via myoendothelial gap junctions or potentially lead to the release of a chemically distinct factor(s). Furthermore, in human isolated coronary arterioles dilator signaling involving EETs and H(2)O(2) may be integrated, being either complimentary or inhibitory depending on the stimulus. With an emphasis on the human coronary microcirculation, this review addresses the diverse and integrated mechanisms by which EETs and H(2)O(2) regulate vessel tone and also examines the hypothesis that myoendothelial microdomain signaling facilitates EDH activity in the human heart.

Indexed as

AnimalsCalcium SignalingCoronary VesselsEicosanoidsEndothelium, VascularGap JunctionsHumansHydrogen PeroxideMuscle, Smooth, VascularMyocardiumVasodilationEicosanoidsHydrogen PeroxideCa2+-activated K+ channelsconnexinscoronary artery diseasecoronary blood flowcytochrome P450 epoxygenasesendothelium-derived hyperpolarizationendothelium-derived hyperpolarizing factorepoxyeicosatrienoic acidsgap junctionshuman coronary microcirculationhydrogen peroxidemitochondrial electron transport chainmyoendothelial signaling microdomainsNADPH oxidasenitric oxidetransient receptor potential channels

Identifiers

PMID26541094
PMCPMC4707990
OpenAlexW2135024493

What OpenQuestion holds

Textmetadata
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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.