Evidence map›Paper›PMID 22326502›Full record

ArticleLife sciences2012

GPER regulates endothelin-dependent vascular tone and intracellular calcium.

Matthias R Meyer, Angela S Field, Nancy L Kanagy, Matthias Barton, Eric R Prossnitz

Open access · hybridAbstract read
In one paragraph

Article in Life sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

41 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Article
  3. GPER expression prevents estrogen-induced urinary retention in obese mice.The Journal of steroid biochemistry and molecular biology · 2024
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Sex differences in vascular aging and impact of GPER deletion.American journal of physiology. Heart and circulatory physiology · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. GPER limits adverse changes to CaFrontiers in physiology · 2022
    Article
  15. Article
  16. Review
  17. G protein-coupled estrogen receptor 1 as a novel regulator of blood pressure.American journal of physiology. Renal physiology · 2020
    Review
  18. 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

5 authors at 2 institutions in 2 countries.

Matthias R MeyerDepartment of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, United States.
Angela S Field
Nancy L Kanagy
Matthias Barton
Eric R Prossnitz
University of New Mexico · USUniversity of Zurich · CH

Funding

UNM HSC Clinical and Translational Science CenterUL1TR001449 · NCATS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI CAMPEN, MATTHEW J, PANDHI, NANCY · 2015 to 2024
$36.9M
University of New Mexico Clinical and Translational Science CenterUL1TR000041 · NCATS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI LARSON, RICHARD S · 2012 to 2014
$9.8M
Development of GPR30-Selective LigandsR01CA127731 · NCI · UNIVERSITY OF NEW MEXICO · PI ARTERBURN, JEFFREY B, OPREA, TUDOR I · 2008 to 2012
$1.7M
Endothelin vasoconstriction in a rat model of sleep apnea-induced hypertension.R01HL082799 · NHLBI · UNIVERSITY OF NEW MEXICO · PI KANAGY, NANCY L · 2007 to 2010
$1.5M
A novel intracellular 7TM estrogen receptor in breastR01CA116662 · NCI · UNIVERSITY OF NEW MEXICO · PI PROSSNITZ, ERIC R · 2006 to 2010
$1.3M
NCATS NIH HHS UL1 TR000041NCATS NIH HHS UL1 TR001449NCI NIH HHS CA127731NCI NIH HHS R01 CA116662NCI NIH HHS R01 CA127731NHLBI NIH HHS HL82799NHLBI NIH HHS R01 HL082799
6 · The paper itself

Abstract

aimsAn increase in intracellular vascular smooth muscle cell calcium concentration (VSMC [Ca(2+)](i)) is essential for endothelin-1 (ET-1)-induced vasoconstriction. Based on previous findings that activation of the G protein-coupled estrogen receptor (GPER) inhibits vasoconstriction in response to ET-1 and regulates [Ca(2+)](i) in cultured VSMC, we investigated whether endogenous GPER regulates ET-1-induced changes in VSMC [Ca(2+)](i) and constriction of intact arteries. MAIN

methodsPressurized carotid arteries of GPER-deficient (GPER(0)) and wildtype (WT) mice were loaded with the calcium indicator fura 2-AM. Arteries were stimulated with the GPER-selective agonist G-1 or solvent followed by exposure to ET-1. Changes in arterial diameter and VSMC [Ca(2+)](i) were recorded simultaneously. Vascular gene expression levels of ET(A) and ET(B) receptors were determined by qPCR. KEY

findingsET-1-dependent vasoconstriction was increased in arteries from GPER(0) compared to arteries from WT mice. Despite the more potent vasoconstriction to ET-1, GPER deficiency was associated with a marked reduction in the ET-1-stimulated VSMC [Ca(2+)](i) increase, suggesting an increase in myofilament force sensitivity to [Ca(2+)](i). Activation of GPER by G-1 had no effect on vasoconstriction or VSMC [Ca(2+)](i) responses to ET-1, and expression levels of ET(A) or ET(B) receptor were unaffected by GPER deficiency. SIGNIFICANCE: These results demonstrate that endogenous GPER inhibits ET-1-induced vasoconstriction, an effect that may be associated with reduced VSMC Ca(2+) sensitivity. This represents a potential mechanism through which GPER could contribute to protective effects of endogenous estrogen in the cardiovascular system.

Indexed as

AnimalsCalciumCarotid ArteriesEndothelin-1Fluorescent DyesFura-2Gene Expression RegulationMaleMiceMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularPolymerase Chain ReactionReceptor, Endothelin AReceptor, Endothelin BReceptors, EstrogenCalciumEndothelin-1Fluorescent DyesFura-2fura-2-amGPER1 protein, mouseReceptor, Endothelin AReceptor, Endothelin BReceptors, EstrogenReceptors, G-Protein-Coupled

Identifiers

PMID22326502
PMCPMC3355219
OpenAlexW1988397302

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Registered trials

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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.