Evidence map›Paper›PMID 21081213›Full record

ReviewAdvances in pharmacology (San Diego, Calif.)2010

The cardiovascular physiology and pharmacology of endothelin-1.

Eric Thorin, Martine Clozel

Open access · greenAbstract readReview
In one paragraph

Review in Advances in pharmacology (San Diego, Calif.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
26.1field-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

36 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
  2. The machinery of healthy vasoconstriction: an overview.Pflugers Archiv : European journal of physiology · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. The importance of comorbidities in ischemic stroke: Impact of hypertension on the cerebral circulation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
    Review
  15. Targeting vascular (endothelial) dysfunction.British journal of pharmacology · 2017
    Review
  16. Review
  17. Review
  18. Review
  19. Lung Circulation.Comprehensive Physiology · 2016
    Review
  20. 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

2 authors at 2 institutions in 2 countries.

Eric ThorinDepartment of Surgery, Montreal Heart Institute, Research Center, Université de Montréal, Montreal, Quebec, Canada.
Martine Clozel
Actelion (Switzerland) · CHMontreal Heart Institute · CA

Funding

CIHR 14496-4CIHR MOP 14496CIHR MOP 89733
6 · The paper itself

Abstract

One year after the discovery in 1980 that the endothelium was obligatory for acetylcholine to relax isolated arteries, it was clearly shown that the endothelium could also promote contraction. In 1988, Dr Yanagisawa's group identified endothelin-1 (ET-1) as the first endothelium-derived contracting factor. The circulating levels of this short (21 amino acids) peptide were quickly determined in humans and it was reported that in most cardiovascular diseases, circulating levels of ET-1 were increased and ET-1 was then recognized as a likely mediator of pathological vasoconstriction in human. The discovery of two receptor subtypes in 1990, ET(A) and ET(B), permitted optimization of bosentan, which entered clinical development in 1993, and was offered to patients with pulmonary arterial hypertension in 2001. In this report, we discuss the physiological and pathophysiological role of endothelium-derived ET-1, the pharmacology of its two receptors, focusing on the regulation of the vascular tone and as much as possible in humans. The coronary bed will be used as a running example, but references to the pulmonary, cerebral, and renal circulation will also be made. Many of the cardiovascular complications associated with aging and cardiovascular risk factors are initially attributable, at least in part, to endothelial dysfunction, particularly dysregulation of the vascular function associated with an imbalance in the close interdependence of NO and ET-1, in which the implication of the ET(B) receptor may be central.

Indexed as

AnimalsCardiovascular Physiological PhenomenaEndothelin-1Endothelin Receptor AntagonistsHumansReceptors, EndothelinEndothelin-1Endothelin Receptor AntagonistsReceptors, Endothelin

Identifiers

PMID21081213
PMCPMC3693982
OpenAlexW1546433028

What Socratic 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 Socratic graph.