Evidence map›Paper›PMID 20817830›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2010

Augmented EDHF signaling in rat uteroplacental vasculature during late pregnancy.

N I Gokina, O Y Kuzina, A M Vance

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2010. 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
2.3field-weighted citation impact, top 11% 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, 56 citations in OpenAlex.

  1. Endothelial Dysfunction in Preeclampsia: Focus on the Uteroplacental Circulation.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Perivascular Adipose Tissue and Uterine Artery Adaptations to Pregnancy.Microcirculation (New York, N.Y. : 1994) · 2024
    Review
  7. Article
  8. CaInternational journal of molecular sciences · 2023
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Vascular mechanisms and molecular targets in hypertensive pregnancy and preeclampsia.American journal of physiology. Heart and circulatory physiology · 2020
    Review
  17. Article
  18. Review
  19. Article
  20. Review
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

3 authors at 1 institution in 1 country.

N I GokinaDept. of Obstetrics, Gynecology, and Reproductive Sciences, College of Medicine, The Univ. of Vermont, Burlington, VT 05405, USA. Natalia.Gokina@uvm.edu
O Y Kuzina
A M Vance
University of Vermont · US

Funding

PPARy and Uterine Vascular Dysfunction in Diabetic PregnancyR01HL088245 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI GOKINA, NATALIA I · 2008 to 2011
$1.4M
Mechanisms of uterine vascular adaptation in pregnancyR01HL067250 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI GOKINA, NATALIA I · 2003 to 2006
$1.2M
NHLBI NIH HHS HL-067250NHLBI NIH HHS HL-088245
6 · The paper itself

Abstract

A successful pregnancy outcome relies on extensive maternal cardiovascular adaptation, including enhanced uteroplacental vasodilator mechanisms. The objective of the present study was to determine the contribution of the endothelium-derived hyperpolarizing factor (EDHF) signaling in pregnancy-enhanced uterine vasodilation, to define the role of Ca(2+)-activated K(+) channels in mediating EDHF effects, and to explore the impact of endothelial Ca(2+) signaling in pregnancy-specific upregulation of EDHF. Fura 2-based measurements of smooth muscle cell (SMC) and endothelial cell cytosolic Ca(2+) concentration ([Ca(2+)](i)) were performed simultaneously with measurements of the diameter of uterine radial arteries from nonpregnant (NP) and late pregnant (LP) rats. Changes in SMC membrane potential of pressurized arteries from LP rats were assessed using glass microelectrodes. After blockade of nitric oxide and prostacyclin production, a cumulative application of ACh induced rapid and effective dilatation of uterine vessels from both NP and LP rats. This vasodilation was associated with SMC hyperpolarization and SMC [Ca(2+)](i) reduction and was abolished by a high-K(+) solution, demonstrating that N(G)-nitro-L-arginine (L-NNA)- and indomethacin-resistant responses are attributable to EDHF. Pregnancy significantly potentiates EDHF-mediated vasodilation in part due to enhanced endothelial Ca(2+) signaling. L-NNA- and indomethacin-resistant responses were insensitive to iberiotoxin but abolished by a combined treatment with apamin and charybdotoxin, supporting the key role of small- and intermediate-conductance K(+) channels in mediating EDHF signaling in the maternal uterine resistance vasculature.

Indexed as

AnimalsApaminBiological FactorsCalcium SignalingCharybdotoxinCyclooxygenase InhibitorsFemaleIndomethacinModels, AnimalNitric Oxide SynthasePlacental CirculationPotassium Channels, Calcium-ActivatedPregnancyPregnancy, AnimalProstaglandin-Endoperoxide SynthasesRatsApaminBiological FactorsCharybdotoxinCyclooxygenase Inhibitorsendothelium-dependent hyperpolarization factorIndomethacinNitric Oxide SynthasePotassium Channels, Calcium-ActivatedProstaglandin-Endoperoxide Synthases

Identifiers

PMID20817830
PMCPMC2993200
OpenAlexW1968165380

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.