Evidence map›Paper›PMID 26101346›Full record

ArticleHypertension (Dallas, Tex. : 1979)2015

Inducible human endothelin-1 overexpression in endothelium raises blood pressure via endothelin type A receptors.

Yohann Rautureau, Suellen C Coelho, Julio C Fraulob-Aquino, Ku-Geng Huo, Asia Rehman, Stefan Offermanns, Pierre Paradis, Ernesto L Schiffrin

Abstract read
PubMed Publisher
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

14 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Endothelin antagonists for hypertension: has their time finally arrived?Clinical science (London, England : 1979) · 2025
    Review
  4. Article
  5. Article
  6. Endothelin System in Hypertension and Chronic Kidney Disease.Hypertension (Dallas, Tex. : 1979) · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The emerging role of endothelin-1 in the pathogenesis of pre-eclampsia.Therapeutic advances in cardiovascular disease · 2016
    Review
  14. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 2 countries.

Yohann RautureauFrom the Hypertension and Vascular Research Unit, Lady Davis Institute for Medical Research (Y.R., S.C.C., J.C.F.-A., K.-G.H., A.R., P.P., E.L.S.) and Department of Medicine, Sir Mortimer B. Davis-Jewish General Hospital (E.L.S.), McGill University, Montreal, Quebec, Canada; and Department of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Nauheim, Germany (S.O.).
Suellen C CoelhoFrom the Hypertension and Vascular Research Unit, Lady Davis Institute for Medical Research (Y.R., S.C.C., J.C.F.-A., K.-G.H., A.R., P.P., E.L.S.) and Department of Medicine, Sir Mortimer B. Davis-Jewish General Hospital (E.L.S.), McGill University, Montreal, Quebec, Canada; and Department of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Nauheim, Germany (S.O.).
Julio C Fraulob-AquinoFrom the Hypertension and Vascular Research Unit, Lady Davis Institute for Medical Research (Y.R., S.C.C., J.C.F.-A., K.-G.H., A.R., P.P., E.L.S.) and Department of Medicine, Sir Mortimer B. Davis-Jewish General Hospital (E.L.S.), McGill University, Montreal, Quebec, Canada; and Department of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Nauheim, Germany (S.O.).
Ku-Geng HuoFrom the Hypertension and Vascular Research Unit, Lady Davis Institute for Medical Research (Y.R., S.C.C., J.C.F.-A., K.-G.H., A.R., P.P., E.L.S.) and Department of Medicine, Sir Mortimer B. Davis-Jewish General Hospital (E.L.S.), McGill University, Montreal, Quebec, Canada; and Department of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Nauheim, Germany (S.O.).
Asia RehmanFrom the Hypertension and Vascular Research Unit, Lady Davis Institute for Medical Research (Y.R., S.C.C., J.C.F.-A., K.-G.H., A.R., P.P., E.L.S.) and Department of Medicine, Sir Mortimer B. Davis-Jewish General Hospital (E.L.S.), McGill University, Montreal, Quebec, Canada; and Department of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Nauheim, Germany (S.O.).
Stefan OffermannsFrom the Hypertension and Vascular Research Unit, Lady Davis Institute for Medical Research (Y.R., S.C.C., J.C.F.-A., K.-G.H., A.R., P.P., E.L.S.) and Department of Medicine, Sir Mortimer B. Davis-Jewish General Hospital (E.L.S.), McGill University, Montreal, Quebec, Canada; and Department of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Nauheim, Germany (S.O.).
Pierre ParadisFrom the Hypertension and Vascular Research Unit, Lady Davis Institute for Medical Research (Y.R., S.C.C., J.C.F.-A., K.-G.H., A.R., P.P., E.L.S.) and Department of Medicine, Sir Mortimer B. Davis-Jewish General Hospital (E.L.S.), McGill University, Montreal, Quebec, Canada; and Department of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Nauheim, Germany (S.O.).
Ernesto L SchiffrinFrom the Hypertension and Vascular Research Unit, Lady Davis Institute for Medical Research (Y.R., S.C.C., J.C.F.-A., K.-G.H., A.R., P.P., E.L.S.) and Department of Medicine, Sir Mortimer B. Davis-Jewish General Hospital (E.L.S.), McGill University, Montreal, Quebec, Canada; and Department of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Nauheim, Germany (S.O.). ernesto.schiffrin@mcgill.ca.
Jewish General Hospital · CA

Funding

Canadian Institutes of Health Research 102606Canadian Institutes of Health Research 37917
6 · The paper itself

Abstract

The mechanisms of blood pressure regulation by endothelin-1 produced by endothelial cells are complex and still unclear. Transgenic mice with endothelium-restricted human endothelin-1 (EDN1) overexpression presented vascular damage but no significant change in blood pressure, which could be because of adaptation to life-long exposure to elevated endothelin-1 levels. We now generated a tamoxifen-inducible endothelium-restricted EDN1 overexpressing transgenic mouse (ieET-1) using Cre/loxP technology. Sixteen days after tamoxifen treatment, ieET-1 mice presented ≥10-fold increase in plasma endothelin-1 (P<0.01) and ≥20 mm Hg elevation in systolic blood pressure (P<0.01), which could be reversed by atrasentan (P<0.05). Endothelin-1 overexpression did not cause vascular or kidney injury or changes in kidney perfusion or function. However, endothelin type A and B receptor expression was differentially regulated in the mesenteric arteries and the kidney. Our results demonstrate using this ieET-1 mouse model that 21 days of induction of endothelin-1 overexpression caused endothelin-1-dependent elevated blood pressure mediated by endothelin type A receptors.

Indexed as

AnimalsAtrasentanBlood PressureDisease Models, AnimalEndothelin-1Endothelium, VascularHumansHypertensionMaleMiceMice, Inbred C57BLMice, TransgenicPyrrolidinesReceptor, Endothelin AReceptor, Endothelin BReceptors, EndothelinAtrasentanEDNRB protein, humanEndothelin-1PyrrolidinesReceptor, Endothelin AReceptor, Endothelin BReceptors, EndothelinTamoxifenblood pressureendothelin-1endothelin receptors type Aendotheliummice, transgenic

Identifiers

PMID26101346
OpenAlexW2140606362

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.