Evidence map›Paper›PMID 26655634›Full record

ArticleScientific reports2015

Antagonism of Nav channels and α1-adrenergic receptors contributes to vascular smooth muscle effects of ranolazine.

Anne Virsolvy, Charlotte Farah, Nolwenn Pertuit, Lingyan Kong, Alain Lacampagne, Cyril Reboul, Franck Aimond, Sylvain Richard

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 30% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Effects of Ranolazine on Vascular Adrenergic Receptors in Rabbit Aorta.International journal of medical sciences · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Improvement of Vascular Insulin Sensitivity by Ranolazine.International journal of molecular sciences · 2023
    Article
  6. Article
  7. Review
  8. Article
  9. 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

8 authors at 3 institutions in 1 country.

Anne VirsolvyPhyMedExp, INSERM U1046, UMR CNRS 9214, Université de Montpellier, Montpellier F-34295, France.
Charlotte FarahAvignon Université, LAPEC EA4278, F-84000, Avignon, France.
Nolwenn PertuitPhyMedExp, INSERM U1046, UMR CNRS 9214, Université de Montpellier, Montpellier F-34295, France.
Lingyan KongPhyMedExp, INSERM U1046, UMR CNRS 9214, Université de Montpellier, Montpellier F-34295, France.
Alain LacampagnePhyMedExp, INSERM U1046, UMR CNRS 9214, Université de Montpellier, Montpellier F-34295, France.
Cyril ReboulAvignon Université, LAPEC EA4278, F-84000, Avignon, France.
Franck AimondPhyMedExp, INSERM U1046, UMR CNRS 9214, Université de Montpellier, Montpellier F-34295, France.
Sylvain RichardPhyMedExp, INSERM U1046, UMR CNRS 9214, Université de Montpellier, Montpellier F-34295, France.
Université d'Avignon et des Pays de Vaucluse · FRPhysiologie et Médecine Expérimentale du Coeur et des Muscles · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ranolazine is a recently developed drug used for the treatment of patients with chronic stable angina. It is a selective inhibitor of the persistent cardiac Na(+) current (INa), and is known to reduce the Na(+)-dependent Ca(2+) overload that occurs in cardiomyocytes during ischemia. Vascular effects of ranolazine, such as vasorelaxation,have been reported and may involve multiple pathways. As voltage-gated Na(+) channels (Nav) present in arteries play a role in contraction, we hypothesized that ranolazine could target these channels. We studied the effects of ranolazine in vitro on cultured aortic smooth muscle cells (SMC) and ex vivo on rat aortas in conditions known to specifically activate or promote INa. We observed that in the presence of the Nav channel agonist veratridine, ranolazine inhibited INa and intracellular Ca(2+) calcium increase in SMC, and arterial vasoconstriction. In arterial SMC, ranolazine inhibited the activity of tetrodotoxin-sensitive voltage-gated Nav channels and thus antagonized contraction promoted by low KCl depolarization. Furthermore, the vasorelaxant effects of ranolazine, also observed in human arteries and independent of the endothelium, involved antagonization of the α1-adrenergic receptor. Combined α1-adrenergic antagonization and inhibition of SMCs Nav channels could be involved in the vascular effects of ranolazine.

Indexed as

Action PotentialsAdrenergic alpha-1 Receptor AntagonistsAnimalsAortaHumansMuscle ContractionMuscle, Smooth, VascularMyocytes, Smooth MuscleRanolazineRatsReceptors, Adrenergic, alpha-1Sodium Channel BlockersUterine ArteryVasodilationVoltage-Gated Sodium ChannelsAdrenergic alpha-1 Receptor AntagonistsRanolazineReceptors, Adrenergic, alpha-1Sodium Channel BlockersVoltage-Gated Sodium Channels

Identifiers

PMID26655634
PMCPMC4674695
OpenAlexW2287972842

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.