Evidence map›Paper›PMID 12922932›Full record

ArticleBritish journal of pharmacology2003

Involvement of Rho-kinase in contraction of guinea-pig aorta induced by prostanoid EP3 receptor agonists.

Winnie W C Shum, Geng-Yun Le, Robert L Jones, Alison M Gurney, Yasuharu Sasaki

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. The deleterious role of the prostaglandin EAmerican journal of physiology. Heart and circulatory physiology · 2020
    Article
  4. PGE2-EP3 signaling exacerbates intracerebral hemorrhage outcomes in 24-mo-old mice.American journal of physiology. Heart and circulatory physiology · 2016
    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

5 authors at 3 institutions in 3 countries.

Winnie W C ShumDepartment of Pharmacology, Faculty of Medicine, Basic Medical Sciences Building, The Chinese University of Hong Kong, Shatin, Hong Kong SAR, China.
Geng-Yun Le
Robert L Jones
Alison M Gurney
Yasuharu Sasaki
Chinese University of Hong Kong · CNKitasato University · JPUniversity of Strathclyde · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. The mechanism of contraction of guinea-pig isolated aorta induced by the prostanoid EP(3) receptor agonist sulprostone (0.1-300 nM) has been investigated. In 60% of the experiments, the sulprostone log concentration-response curve (maximum=15-40% of 100 nM U-46619 response; low-responders) was unaffected by the removal of extracellular Ca(2+), blockade of L-type Ca(2+) channels with nifedipine and depletion of internal Ca(2+) stores. In the remaining preparations (35-65% of 100 nM U-46619 response; high-responders), contractions to higher sulprostone concentrations showed a nifedipine-sensitive component, which was enhanced by charybdotoxin. 2. In Ca(2+)-free Krebs solution, established contractions to 300 nM sulprostone were abolished by the Rho-kinase inhibitors H-1152, Y-27632 and HA-1077 (IC(50) values=190, 770 and 2030 nM). The PKA/Rho-kinase inhibitor H-89 (10 nM-10 micro M) caused enhancement progressing to inhibition. The selective PKC inhibitor Ro 32-0432 (3 micro M) had no effect, while staurosporine, recently shown to be a potent Rho-kinase inhibitor, abolished sulprostone responses (IC(50) approximately 47 nM), but its action was slow. The MAP kinase inhibitors SB 202190, SB 203580 and PD 80958 produced little inhibition. 3. In normal Krebs solution, H-1152 and Y-27632 abolished established contractions to 300 nM sulprostone and 1 micro M phenylephrine, and partially inhibited 10 micro M phenylephrine and 50 mM K(+) responses. 4. The results are discussed in relation to the reported potencies of the protein kinase inhibitors in enzyme assays. Activation of the Rho-kinase pathway appears to be a primary mechanism of contraction induced by EP(3) receptor agonists in guinea-pig aorta.

Indexed as

AnimalsAorta, ThoracicCalcium Channel BlockersCalcium Channels, L-TypeDinoprostoneDose-Response Relationship, DrugEnzyme InhibitorsGuinea PigsIntracellular Signaling Peptides and ProteinsIn Vitro TechniquesMaleMuscle ContractionMuscle, Smooth, VascularNifedipineProtein Serine-Threonine KinasesReceptors, Prostaglandin ECalcium Channel BlockersCalcium Channels, L-TypeDinoprostoneEnzyme InhibitorsIntracellular Signaling Peptides and ProteinsNifedipineProtein Serine-Threonine KinasesReceptors, Prostaglandin EReceptors, Prostaglandin E, EP3 Subtyperho-Associated Kinasessulprostone

Identifiers

PMID12922932
PMCPMC1573987
OpenAlexW2016145225

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.