Evidence map›Paper›PMID 19154435›Full record

ReviewBritish journal of pharmacology2009

Endothelium-dependent contractions in SHR: a tale of prostanoid TP and IP receptors.

Michel Félétou, Tony J Verbeuren, Paul M Vanhoutte

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
11.8field-weighted citation impact, top 1% 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

55 citing papers in PubMed, 159 citations in OpenAlex.

  1. Trial
  2. The machinery of healthy vasoconstriction: an overview.Pflugers Archiv : European journal of physiology · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. An Overview of NO Signaling Pathways in Aging.Molecules (Basel, Switzerland) · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Crossing signals: bioactive lipids in the microvasculature.American journal of physiology. Heart and circulatory physiology · 2020
    Review
  13. Prostaglandins as the Agents That Modulate the Course of Brain Disorders.Degenerative neurological and neuromuscular disease · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Endothelial prostacyclin protects the kidney from ischemia-reperfusion injury.Pflugers Archiv : European journal of physiology · 2019
    Article
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 2 institutions in 2 countries.

Michel FélétouDepartment of Angiology, Institut de Recherches Servier, Suresnes, France. michel.feletou@fr.netgrs.com
Tony J Verbeuren
Paul M Vanhoutte
Servier (France) · FRUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the aorta of spontaneously hypertensive rats (SHR), the endothelial dysfunction is due to the release of endothelium-derived contracting factors (EDCFs) that counteract the vasodilator effect of nitric oxide, with no or minor alteration of its production. The endothelium-dependent contractions elicited by acetylcholine (ACh) involve an increase in endothelial [Ca(2+)](i), the production of reactive oxygen species, the activation of endothelial cyclooxygenase-1, the diffusion of EDCF and the subsequent stimulation of smooth muscle cell TP receptors. The EDCFs released by ACh have been identified as PGH(2) and paradoxically prostacyclin. Prostacyclin generally acts as an endothelium-derived vasodilator, which, by stimulating IP receptors, produces hyperpolarization and relaxation of the smooth muscle and inhibits platelet aggregation. In the aorta of SHR and Wistar-Kyoto rats, prostacyclin is the principal metabolite of arachidonic acid released by ACh. However, in SHR aorta, prostacyclin does not produce relaxations but activates the TP receptors on vascular smooth muscle cells and produces contraction. The IP receptor is not functional in the aortic smooth muscle cells of SHR as early as 12 weeks of age, but its activity is not reduced in platelets. Therefore, prostacyclin in the rule protects the vascular wall, but in the SHR aorta it can contribute to endothelial dysfunction. Whether or not prostacyclin plays a detrimental role as an EDCF in other animal models or in human remains to be demonstrated. Nevertheless, because EDCFs converge to activate TP receptors, selective antagonists of this receptor, by preventing endothelium-dependent contractions, curtail the endothelial dysfunction in diseases such as hypertension and diabetes.

Indexed as

AcetylcholineAnimalsAortaEndothelium, VascularHumansHypertensionRatsRats, Inbred SHRReceptors, EpoprostenolReceptors, ProstaglandinReceptors, ThromboxaneVasoconstrictionAcetylcholinePtgir protein, ratReceptors, EpoprostenolReceptors, ProstaglandinReceptors, Thromboxane

Identifiers

PMID19154435
PMCPMC2697704
OpenAlexW2017343731

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.