Evidence map›Paper›PMID 24111896›Full record

ArticleBritish journal of pharmacology2014

KV 7 channels are involved in hypoxia-induced vasodilatation of porcine coronary arteries.

E R Hedegaard, B D Nielsen, A Kun, A D Hughes, C Krøigaard, S Mogensen, V V Matchkov, O Fröbert, U Simonsen

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 76 citations in OpenAlex.

  1. HBasic research in cardiology · 2025
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  9. Potential Effects of Natural HBiomolecules · 2022
    Review
  10. KCurrent topics in membranes · 2022
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Kv7 Channels and Excitability Disorders.Handbook of experimental pharmacology · 2021
    Article
  18. Article
  19. Article
  20. Alteration of purinergic signaling in diabetes: Focus on vascular function.Journal of molecular and cellular cardiology · 2020
    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

9 authors at 4 institutions in 3 countries.

E R HedegaardDepartment of Biomedicine, Pulmonary and Cardiovascular Pharmacology, University of Aarhus, Aarhus, Denmark.
B D Nielsen
A Kun
A D Hughes
C Krøigaard
S Mogensen
V V Matchkov
O Fröbert
U Simonsen
Aarhus University · DKAarhus University Hospital · DKNational Institutes of Health · USÖrebro University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeHypoxia causes vasodilatation of coronary arteries, but the underlying mechanisms are poorly understood. We hypothesized that hypoxia reduces intracellular Ca(2+) concentration ([Ca(2+)](i)) by opening of K channels and release of H₂S. EXPERIMENTAL APPROACH: Porcine coronary arteries without endothelium were mounted for measurement of isometric tension and [Ca(2+)](i), and the expression of voltage-gated K channels K(V)7 channels (encoded by KCNQ genes) and large-conductance calcium-activated K channels (K(Ca)1.1) was examined. Voltage clamp assessed the role of K(V)7 channels in hypoxia. KEY

resultsGradual reduction of oxygen concentration from 95 to 1% dilated the precontracted coronary arteries and this was associated with reduced [Ca(2+)](i) in PGF(2α) (10 μM)-contracted arteries whereas no fall in [Ca(2+)](i) was observed in 30 mM K-contracted arteries. Blockers of ATP-sensitive voltage-gated potassium channels and K(Ca)1.1 inhibited hypoxia-induced dilatation in PGF2α -contracted arteries; this inhibition was more marked in the presence of the K(v)7 channel blockers, XE991 and linopirdine, while a K(V)7.1 blocker, failed to change hypoxic vasodilatation. XE991 also inhibited H₂S- and adenosine-induced vasodilatation. PCR revealed the expression of K(V)7.1, K(V)7.4, K(V)7.5 and K(Ca)1.1 channels, and K(Ca)1.1, K(V)7.4 and K(V)7.5 were also identified by immunoblotting. Voltage clamp studies showed the XE991-sensitive current was more marked in hypoxic conditions.

conclusionThe K(V)7.4 and K(V)7.5 channels, which we identified in the coronary arteries, appear to have a major role in hypoxia-induced vasodilatation. The voltage clamp results further support the involvement of K(V)7 channels in this vasodilatation. Activation of these K(V)7 channels may be induced by H₂S and adenosine.

Indexed as

VasodilationAdenosineAnimalsCalcium SignalingCoronary VesselsDose-Response Relationship, DrugHydrogen SulfideHypoxiaKCNQ Potassium ChannelsLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMembrane PotentialsMuscle, Smooth, VascularOxygenPotassium Channel BlockersSignal TransductionSwineAdenosineHydrogen SulfideKCNQ Potassium ChannelsLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsOxygenPotassium Channel BlockersVasodilator AgentsadenosinecalciumcoronaryH2ShypoxiaKV7potassium channelsvasodilatation

Identifiers

PMID24111896
PMCPMC3874697
OpenAlexW1733067719

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.