Evidence map›Paper›PMID 30458188›Full record

ArticleSteroids2019

Equilin displays similar endothelium-independent vasodilator potential to 17β-estradiol regardless of lower potential to inhibit calcium entry.

Fernando P Filgueira, Núbia S Lobato, Denise L Nascimento, Graziela S Ceravolo, Fernanda R C Giachini, Victor V Lima, Ana Paula Dantas, Zuleica B Fortes, R Clinton Webb, Rita C Tostes and 1 more

Open access · greenAbstract read
In one paragraph

Article in Steroids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 35% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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

11 authors at 6 institutions in 3 countries.

Fernando P FilgueiraDepartment of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, Brazil; Department of Physiology, Augusta University, Augusta, GA, USA; Faculty of Medicine, Institute of Health Sciences, Federal University of Jatai, Jatai, GO, Brazil. Electronic address: fpfilgueira@yahoo.com.br.
Núbia S LobatoDepartment of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, Brazil; Department of Physiology, Augusta University, Augusta, GA, USA; Faculty of Medicine, Institute of Health Sciences, Federal University of Jatai, Jatai, GO, Brazil.
Denise L NascimentoFaculty of Medicine, Institute of Health Sciences, Federal University of Jatai, Jatai, GO, Brazil.
Graziela S CeravoloDepartment of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, Brazil; Department of Physiological Sciences, Biological Sciences Center, State University of Londrina, Londrina, PR, Brazil.
Fernanda R C GiachiniDepartment of Physiology, Augusta University, Augusta, GA, USA; Institute of Biological and Health Sciences, Federal University of Mato Grosso, Barra do Garças, MT, Brazil.
Victor V LimaDepartment of Physiology, Augusta University, Augusta, GA, USA; Institute of Biological and Health Sciences, Federal University of Mato Grosso, Barra do Garças, MT, Brazil; Department of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, SP, Brazil.
Ana Paula DantasExperimental Cardiology, Institut Clínic Cardiovascular, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain.
Zuleica B FortesDepartment of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, Brazil.
R Clinton WebbDepartment of Physiology, Augusta University, Augusta, GA, USA.
Rita C TostesDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, SP, Brazil.
Maria Helena C CarvalhoDepartment of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, Brazil.
Universidade de São Paulo · BRAugusta University · USUniversidade Federal de Jataí · BRUniversidade Federal de Mato Grosso · BRConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESUniversidade Estadual de Londrina · BR

Funding

Toll-like receptor 9 activation by mitochondrial DNA causes vascular injury in hypertensionP01HL134604 · NHLBI · AUGUSTA UNIVERSITY · PI BRANDS, MICHAEL W. · 2017 to 2021
$9.4M
NHLBI NIH HHS P01 HL134604
6 · The paper itself

Abstract

Conjugated equine estrogens (CEE) have been widely used by women who seek to relieve symptoms of menopause. Despite evidence describing protective effects against risk factors for cardiovascular diseases by naturally occurring estrogens, little is known about the vascular effects of equilin, one of the main components of CEE and not physiologically present in women. In this regard, the present study aims to compare the vascular effects of equilin in an experimental model of hypertension with those induced by 17β-estradiol. Resistance mesenteric arteries from female spontaneously hypertensive rats (SHR) were used for recording isometric tension in a small vessel myograph. As effectively as 17β-estradiol, equilin evoked a concentration-dependent relaxation in mesenteric arteries from female SHRs contracted with KCl, U46619, PDBu or ET-1. Equilin-induced vasodilation does not involve classical estrogen receptor activation, since the estrogen receptor antagonist (ICI 182,780) failed to inhibit relaxation in U46619-precontracted mesenteric arteries. Vasorelaxation was not affected by either endothelium removal or by inhibiting the release or action of endothelium-derived factors. Incubation with L-NAME (NOS inhibitor), ODQ (guanylyl cyclase inhibitor) or KT5823 (inhibitor of protein kinase G) did not affect equilin-induced relaxation. Similarly, indomethacin (COX inhibitor) or blockage of potassium channels with tetraethylammonium, glibenclamide, 4-aminopyridine, or ouabain did not affect equilin-induced relaxation. Inhibitors of adenylyl cyclase SQ22536 or protein kinase A (KT5720) also had no effects on equilin-induced relaxation. While 17β-estradiol inhibited calcium (Ca

Indexed as

AnimalsCalciumEndoplasmic ReticulumEquilinEstradiolFemaleRatsRats, Inbred SHRVasodilationVasodilator AgentsCalciumEquilinEstradiolVasodilator Agents17β-EstradiolCalcium channelEquilinMesenteric arteriesVasorelaxation

Identifiers

PMID30458188
PMCPMC6984400
OpenAlexW2901095927

What OpenQuestion 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 OpenQuestion graph.