Evidence map›Paper›PMID 27789473›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2016

Kv7 Channel Activation Underpins EPAC-Dependent Relaxations of Rat Arteries.

Jennifer B Stott, Vincenzo Barrese, Iain A Greenwood

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 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
3.3field-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

26 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  14. Pirfenidone Is a Vasodilator: Involvement of KFrontiers in pharmacology · 2020
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  17. Striatal Cholinergic Interneurons Are a Novel Target of Corticotropin Releasing Factor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  18. Article
  19. Reporting Sex and Sex Differences in Preclinical Studies.Arteriosclerosis, thrombosis, and vascular biology · 2018
    Article
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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 1 institution in 1 country.

Jennifer B StottFrom the Vascular Biology Research Group, Institute for Cardiovascular and Cell Sciences, St George's University of London, UK.
Vincenzo BarreseFrom the Vascular Biology Research Group, Institute for Cardiovascular and Cell Sciences, St George's University of London, UK.
Iain A GreenwoodFrom the Vascular Biology Research Group, Institute for Cardiovascular and Cell Sciences, St George's University of London, UK. grenwood@sgul.ac.uk.
St George's, University of London · GB

Funding

British Heart Foundation PG/12/63/29824Medical Research Council MR/K019074/1
6 · The paper itself

Abstract

objectiveTo establish the role of Kv7 channels in EPAC (exchange protein directly activated by cAMP)-dependent relaxations of the rat vasculature and to investigate whether this contributes to β-adrenoceptor-mediated vasorelaxations. APPROACH AND

resultsIsolated rat renal and mesenteric arteries (RA and MA, respectively) were used for isometric tension recording to study the relaxant effects of a specific EPAC activator and the β-adrenoceptor agonist isoproterenol in the presence of potassium channel inhibitors and cell signaling modulators. Isolated myocytes were used in proximity ligation assay studies to detect localization of signaling intermediaries with Kv7.4 before and after cell stimulation. Our studies showed that the EPAC activator (8-pCPT-2Me-cAMP-AM) produced relaxations and enhanced currents of MA and RA that were sensitive to linopirdine (Kv7 inhibitor). Linopirdine also inhibited isoproterenol-mediated relaxations in both RA and MA. In the MA, isoproterenol relaxations were sensitive to EPAC inhibition, but not protein kinase A inhibition. In contrast, isoproterenol relaxations in RA were attenuated by protein kinase A but not by EPAC inhibition. Proximity ligation assay showed a localization of Kv7.4 with A-kinase anchoring protein in both vessels in the basal state, which increased only in the RA with isoproterenol stimulation. In the MA, but not the RA, a localization of Kv7.4 with both Rap1a and Rap2 (downstream of EPAC) increased with isoproterenol stimulation.

conclusionsEPAC-dependent vasorelaxations occur in part via activation of Kv7 channels. This contributes to the isoproterenol-mediated relaxation in mesenteric, but not renal, arteries.

Indexed as

VasodilationAdrenergic beta-AgonistsA Kinase Anchor ProteinsAnimalsCyclic AMP-Dependent Protein KinasesDose-Response Relationship, DrugGuanine Nucleotide Exchange FactorsHEK293 CellsHumansIn Vitro TechniquesKCNQ Potassium ChannelsMaleMembrane PotentialsMesenteric ArteriesPotassium Channel BlockersProtein Kinase InhibitorsAdrenergic beta-AgonistsA Kinase Anchor ProteinsCyclic AMP-Dependent Protein KinasesGuanine Nucleotide Exchange FactorsKcnq4 protein, ratKCNQ Potassium ChannelsPotassium Channel BlockersProtein Kinase Inhibitorsrap1 GTP-Binding ProteinsRapgef3 protein, ratVasodilator Agentscyclic nucleotideisoproterenolK channelsignaling pathwaysvascular smooth muscle

Identifiers

PMID27789473
PMCPMC5467728
OpenAlexW2550110199

What OpenQuestion holds

Textmetadata
LicenceTDM
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.