Evidence map›Paper›PMID 21791623›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2011

Activation of G protein-coupled estrogen receptor induces endothelium-independent relaxation of coronary artery smooth muscle.

Xuan Yu, Handong Ma, Scott A Barman, Alexander T Liu, Minga Sellers, John N Stallone, Eric R Prossnitz, Richard E White, Guichun Han

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
7.2field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 97 citations in OpenAlex.

  1. Review
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  18. Targeting BKCNS drugs · 2020
    Review
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  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Xuan YuMichael E. DeBakey Institute-Division of Women's Health, Texas A & M University, College Station, Texas, 77843, USA.
Handong Ma
Scott A Barman
Alexander T Liu
Minga Sellers
John N Stallone
Eric R Prossnitz
Richard E White
Guichun Han
Augusta University Health · USTexas A&M University · USUNM Comprehensive Cancer Center

Funding

PKC Signaling in cAMP-Induced Pulmonary VasodilationR01HL068026 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI BARMAN, SCOTT A · 2001 to 2010
$2.3M
NONGENOMIC MECHANISMS OF ANDROGENS IN THE VASCULAR WALLR01HL080402 · NHLBI · TEXAS A&M AGRILIFE RESEARCH · PI STALLONE, JOHN NICHOLAS · 2006 to 2009
$1.4M
Estrogen dual effects on coronary arteriesR01HL073890 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI WHITE, RICHARD E · 2005 to 2008
$1.3M
NHLBI NIH HHS HL-068026NHLBI NIH HHS HL-073890NHLBI NIH HHS HL-080402
6 · The paper itself

Abstract

Estrogens can either relax or contract arteries via rapid, nongenomic mechanisms involving classic estrogen receptors (ER). In addition to ERα and ERβ, estrogen may also stimulate G protein-coupled estrogen receptor 1 (GPER) in nonvascular tissue; however, a potential role for GPER in coronary arteries is unclear. The purpose of this study was to determine how GPER activity influenced coronary artery reactivity. In vitro isometric force recordings were performed on endothelium-denuded porcine arteries. These studies were augmented by RT-PCR and single-cell patch-clamp experiments. RT-PCR and immunoblot studies confirmed expression of GPER mRNA and protein, respectively, in smooth muscle from either porcine or human coronary arteries. G-1, a selective GPER agonist, produced a concentration-dependent relaxation of endothelium-denuded porcine coronary arteries in vitro. This response was attenuated by G15, a GPER-selective antagonist, or by inhibiting large-conductance calcium-activated potassium (BK(Ca)) channels with iberiotoxin, but not by inhibiting NO signaling. Last, single-channel patch-clamp studies demonstrated that G-1 stimulates BK(Ca) channel activity in intact smooth muscle cells from either porcine or human coronary arteries but had no effect on channels isolated in excised membrane patches. In summary, GPER activation relaxes coronary artery smooth muscle by increasing potassium efflux via BK(Ca) channels and requires an intact cellular signaling mechanism. This novel action of estrogen-like compounds may help clarify some of the controversy surrounding the vascular effects of estrogens.

Indexed as

AnimalsCalciumCells, CulturedCoronary VesselsEndothelium, VascularEstradiolHumansLarge-Conductance Calcium-Activated Potassium ChannelsMuscle RelaxationMuscle, Smooth, VascularMyocytes, Smooth MuscleNitric OxideReceptors, EstrogenReceptors, G-Protein-CoupledSwineUp-RegulationCalciumEstradiolGPER1 protein, humanLarge-Conductance Calcium-Activated Potassium ChannelsNitric OxideReceptors, EstrogenReceptors, G-Protein-Coupled

Identifiers

PMID21791623
PMCPMC3213995
OpenAlexW1979986181

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.