Evidence map›Paper›PMID 21985802›Full record

ArticleJournal of vascular research2012

Endothelial-derived hyperpolarization factor (EDHF) contributes to PlGF-induced dilation of mesenteric resistance arteries from pregnant rats.

Maurizio Mandalà, Natalia Gokina, Carolyn Barron, George Osol

Open access · bronzeAbstract read
In one paragraph

Article in Journal of vascular research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Metabolic abnormalities and obesity's impact on the risk for developing preeclampsia.American journal of physiology. Regulatory, integrative and comparative physiology · 2017
    Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Vascular mechanisms and molecular targets in hypertensive pregnancy and preeclampsia.American journal of physiology. Heart and circulatory physiology · 2020
    Review
  10. Article
  11. Placental growth factor blunts uterine artery responses to angiotensin II.BJOG : an international journal of obstetrics and gynaecology · 2019
    Article
  12. Article
  13. Review
  14. Matrix Metalloproteinases in Normal Pregnancy and Preeclampsia.Progress in molecular biology and translational science · 2017
    Review
  15. Article
  16. Article
  17. Review
  18. The SK3 channel promotes placental vascularization by enhancing secretion of angiogenic factors.American journal of physiology. Endocrinology and metabolism · 2014
    Article
  19. 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

4 authors at 1 institution in 1 country.

Maurizio MandalàDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Vermont, College of Medicine, Burlington, Vt. 05405, USA. maurizio.mandala @ uvm.edu
Natalia Gokina
Carolyn Barron
George Osol
University of Vermont · US

Funding

VERGFR-1 in the Uterine Circulation During PregnancyR01HL079253 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI OSOL, GEORGE J · 2008 to 2011
$1.5M
NHLBI NIH HHS HL79253NHLBI NIH HHS R01 HL079253
6 · The paper itself

Abstract

The aim of this study was to investigate the cellular mechanism involved in the potent vasodilatory action of PlGF on mesenteric resistance arteries from pregnant rats. PlGF (3 nM) induced a vasodilation of 64 ± 3.8% that was completely abolished by endothelial denudation. Significant dilation (28 ± 4.0%) remained, however, in the presence of nitric oxide synthase and cyclooxygenase inhibition, and was associated with significant reductions in vascular smooth muscle cell calcium. Absence of dilation in potassium-depolarizing solution (30 mM) confirmed its dependence on endothelial-derived hyperpolarization factor. Subsequent studies established that vasodilation was abolished by pharmacologic inhibition of SK(Ca) (apamin) and BK(Ca) (iberiotoxin) but not IK(Ca) (tram-34) potassium channels. In summary, PlGF acts through the release of a combination of endothelium-derived relaxation factors. Based on the results of potassium channel blockade, we suggest that it induces endothelial hyperpolarization via SK(Ca) channel activation; this, in turn, leads to the release of a diffusible mediator that activates vascular smooth muscle BK(Ca) channels, hyperpolarization and vasodilation. This is the first study to identify the mechanism for PlGF/VEGFR-1 resistance artery dilation in the pregnant state, whose attenuation likely contributes to the systemic hypertension characteristic of pre- eclampsia.

Indexed as

AcetylcholineAnimalsApaminBiological FactorsCalciumCharybdotoxinFemaleMesenteric ArteriesNG-Nitroarginine Methyl EsterPlacenta Growth FactorPotassium Channels, Calcium-ActivatedPregnancyPregnancy, AnimalPregnancy ProteinsRatsRats, Sprague-DawleyAcetylcholineApaminBiological FactorsCalciumCharybdotoxinendothelium-dependent hyperpolarization factorNG-Nitroarginine Methyl EsterPgf protein, ratPlacenta Growth FactorPotassium Channels, Calcium-ActivatedPregnancy ProteinsVascular Endothelial Growth Factor Receptor-1

Identifiers

PMID21985802
PMCPMC3221268
OpenAlexW2048825242

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.