Evidence map›Paper›PMID 16715115›Full record

ArticleBritish journal of pharmacology2006

The levosimendan metabolite OR-1896 elicits vasodilation by activating the K(ATP) and BK(Ca) channels in rat isolated arterioles.

Nóra Erdei, Zoltán Papp, Piero Pollesello, István Edes, Zsolt Bagi

Open access · bronzeAbstract readEvaluation Study
In one paragraph

Article in British journal of pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 2 pooled it
2.6field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 79 citations in OpenAlex.

  1. Repetitive infusion of levosimendan in patients with chronic heart failure: a meta-analysis.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Pooled it
  2. Intermittent levosimendan improves mid-term survival in chronic heart failure patients: meta-analysis of randomised trials.Clinical research in cardiology : official journal of the German Cardiac Society · 2014
    Pooled it
  3. Article
  4. Article
  5. Review
  6. The medical treatment of cardiogenic shock.Journal of intensive medicine · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. BKCardiovascular drugs and therapy · 2021
    Article
  12. Review
  13. Observational
  14. Levosimendan Efficacy and Safety: 20 Years of SIMDAX in Clinical Use.Journal of cardiovascular pharmacology · 2020
    Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Targeting the sarcomere to correct muscle function.Nature reviews. Drug discovery · 2015
    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

5 authors at 1 institution in 2 countries.

Nóra ErdeiDivision of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen H-4004, Hungary.
Zoltán Papp
Piero Pollesello
István Edes
Zsolt Bagi
University of Debrecen · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. We characterized the vasoactive effects of OR-1896, the long-lived metabolite of the inodilator levosimendan, in coronary and skeletal muscle microvessels. 2. The effect of OR-1896 on isolated, pressurized (80 mmHg) rat coronary and gracilis muscle arteriole (approximately 150 microm) diameters was investigated by videomicroscopy. 3. OR-1896 elicited concentration-dependent (1 nM-10 microM) dilations in coronary (maximal dilation: 66+/-6%, relative to that in Ca2+-free solutions; pD2: 7.16+/-0.42) and gracilis muscle arterioles (maximal dilation: 73+/-4%; pD2: 6.71+/-0.42), these dilations proving comparable to those induced by levosimendan (1 nM-10 microM) in coronary (maximal dilation: 83+/-6%; pD2: 7.06+/-0.14) and gracilis muscle arterioles (maximal dilation: 73+/-12%; pD2: 7.05+/-0.1). 4. The maximal dilations in response to OR-1896 were significantly (P<0.05) attenuated by the nonselective K+ channel inhibitor tetraethylammonium (1 mM) in coronary (to 34+/-9%) and gracilis muscle arterioles (to 28+/-6%). 5. Glibenclamide (5 or 10 microM), a selective ATP-sensitive K+ channel (KATP) blocker, elicited a greater reduction of OR-1896-induced dilations in skeletal muscle arterioles than in coronary microvessels. 6. Conversely, the selective inhibition of the large conductance Ca2+-activated K+ channels (BK(Ca)) with iberiotoxin (100 nM) significantly reduced the OR-1896-induced maximal dilation in coronary arterioles (to 21+/-6%), but was ineffective in skeletal muscle arterioles (72+/-8%). 7. Accordingly, OR-1896 elicits a substantial vasodilation in coronary and skeletal muscle arterioles, by activating primarily BK(Ca) and K(ATP) channels, respectively, and it is suggested that OR-1896 contributes to the long-term hemodynamic effects of levosimendan.

Indexed as

AcetamidesAnimalsArteriolesCoronary VesselsHydrazonesLarge-Conductance Calcium-Activated Potassium ChannelsMaleMuscle, SkeletalPotassium ChannelsPyridazinesRatsRats, WistarSimendanVasodilationVasodilator AgentsAcetamidesHydrazonesLarge-Conductance Calcium-Activated Potassium Channelsmitochondrial K(ATP) channelN-(4-(4-methyl-6-oxo-1,4,5,6-tetrahydropyridazin-3-yl)phenyl)acetamidePotassium ChannelsPyridazinesSimendanVasodilator Agents

Identifiers

PMID16715115
PMCPMC1751872
OpenAlexW1580601226

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.