Evidence map›Paper›PMID 21222646›Full record

ReviewCurrent molecular pharmacology2011

Modulators of the vascular endothelin receptor in blood pressure regulation and hypertension.

Raouf A Khalil

Open access · greenAbstract readReview
In one paragraph

Review in Current molecular pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. U0126 attenuates cerebral vasoconstriction and improves long-term neurologic outcome after stroke in female rats.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015
    Article
  15. Review
  16. Article
  17. Mutation of Plekha7 attenuates salt-sensitive hypertension in the rat.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  18. Article
  19. Antihypertensive action of allantoin in animals.BioMed research international · 2014
    Article
  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

1 author at 1 institution in 1 country.

Raouf A KhalilVascular Surgery Research Laboratory, Division of Vascular and Endovascular Surgery, Brigham and Women’s Hospital, and Harvard Medical School, Boston, Massachusetts 02115, USA. raouf_khalil@hms.harvard.edu
Brigham and Women's Hospital · US

Funding

Vascular Mechanisms in Pregnancy-Induced HypertensionR01HL065998 · NHLBI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI KHALIL, RAOUF A · 2002 to 2016
$4.3M
Vascular Protective Role of Endothelin B ReceptorsR01HL070659 · NHLBI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI KHALIL, RAOUF A. · 2003 to 2006
$1.2M
Role of Endothelin B Receptor in Vascular Protection in FemalesR21HL098724 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI KHALIL, RAOUF A · 2010 to 2011
$481k
Vascular Angiotensin Type-2 Receptor in Normal and Hypertensive PregnancyR03HD060702 · NICHD · BRIGHAM AND WOMEN'S HOSPITAL · PI KHALIL, RAOUF A · 2009 to 2010
$172k
NHLBI NIH HHS HL-65998NHLBI NIH HHS HL-70659NHLBI NIH HHS HL-98724NHLBI NIH HHS R01 HL065998NHLBI NIH HHS R01 HL070659NHLBI NIH HHS R21 HL098724NICHD NIH HHS HD-60702NICHD NIH HHS R03 HD060702
6 · The paper itself

Abstract

Endothelin (ET) is one of the most investigated molecules in vascular biology. Since its discovery two decades ago, several ET isoforms, receptors, signaling pathways, agonists and antagonists have been identified. ET functions as a potent endothelium-derived vasoconstrictor, but could also play a role in vascular relaxation. In endothelial cells, preproET and big ET are cleaved by ET converting enzymes into ET-1, -2, -3 and -4. These ET isoforms bind with different affinities to ET(A) and ET(B) receptors in vascular smooth muscle (VSM), and in turn increase [Ca(2+)](i), protein kinase C and mitogen-activated protein kinase and other signaling pathways of VSM contraction and cell proliferation. ET also binds to endothelial ET(B) receptors and stimulates the release of nitric oxide, prostacyclin and endothelium-derived hyperpolarizing factor. ET, via endothelial ET(B) receptor, could also promote ET re-uptake and clearance. While the effects of ET on vascular reactivity and growth have been thoroughly examined, its role in the regulation of blood pressure and the pathogenesis of hypertension is not clearly established. Elevated plasma and vascular tissue levels of ET have been identified in salt-sensitive hypertension and in moderate to severe hypertension, and ET receptor antagonists have been shown to reduce blood pressure to variable extents in these forms of hypertension. The development of new pharmacological and genetic tools could lead to more effective and specific modulators of the vascular ET system for treatment of hypertension and related cardiovascular disease.

Indexed as

Blood PressureEndothelial CellsEndothelin Receptor AntagonistsEndothelinsHumansHypertensionMuscle, Smooth, VascularProtein IsoformsReceptors, EndothelinSignal TransductionEndothelin Receptor AntagonistsEndothelinsProtein IsoformsReceptors, Endothelin

Identifiers

PMID21222646
PMCPMC3134623
OpenAlexW2062105681

What Socratic holds

Textmetadata
LicenceTDM
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.