Evidence map›Paper›PMID 24793048›Full record

ArticlePflugers Archiv : European journal of physiology2015

Hydrogen sulfide impairs shear stress-induced vasodilation in mouse coronary arteries.

Qiang Chai, Tong Lu, Xaio-Li Wang, Hon-Chi Lee

Abstract read
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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

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  17. Vasoconstriction triggered by hydrogen sulfide: Evidence for NaBiochemistry and biophysics reports · 2017
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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 3 institutions in 2 countries.

Qiang ChaiDivision of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic, Rochester, MN, 55905, USA, qiang.chai@hotmail.com.
Tong Lu
Xaio-Li Wang
Hon-Chi Lee
Mayo Clinic · USMayo Clinic in Arizona · USWinnMed · US

Funding

Type 2 Diabetes and Vascular BK Channel RegulationR01HL074180 · NHLBI · MAYO CLINIC ROCHESTER · PI LEE, HON-CHI · 2003 to 2018
$4.8M
Endothelial BK Channel Regulation by Caveolae TargetingR01HL080118 · NHLBI · MAYO CLINIC ROCHESTER · PI LEE, HON-CHI · 2006 to 2010
$1.8M
Regulation of Vascular BK Channels in DiabetesR56HL074180 · NHLBI · MAYO CLINIC ROCHESTER · PI LEE, HON-CHI · 2008 to 2008
$378k
NHLBI NIH HHS HL074180NHLBI NIH HHS HL080118NHLBI NIH HHS R01 HL074180
6 · The paper itself

Abstract

Hydrogen sulfide has emerged as an important endothelium-dependent vasodilator, but its role in shear stress-mediated dilation of coronary arteries is unclear. We examined the role of H2S on shear stress-mediated dilation of isolated mouse coronary arteries. In these vessels, Na2S produced concentration-dependent dilation, which was significantly inhibited by iberiotoxin and by 4-aminopyridine. In addition, BK and Kv currents in mouse coronary smooth muscle cells were directly activated by Na2S, suggesting that H2S produced vasodilation through BK and Kv channel activation. Using a pressure servo controller system, freshly isolated mouse coronary arteries were subjected to physiological levels of shear stress (1 to 25 dynes/cm(2)) and produced graded dilatory responses, but such effects were diminished in the presence of 100 μM Na2S. Pre-incubation with the cystathionine γ-lyase inhibitor, D,L-propargylglycine (PPG), resulted in a paradoxical augmentation of shear stress-mediated vasodilation. However, in the presence of L-NAME or in coronary arteries from eNOS knockout mice, PPG inhibited shear stress-mediated vasodilation, suggesting an interaction between NO and H2S signaling. Na2S inhibited eNOS activity in cultured mouse aortic endothelial cells and reduced the level of phospho-eNOS(serine 1177). These results suggest that both NO and H2S are important shear stress-mediated vasodilators in mouse coronary arteries but there is a complex interaction between these two signaling pathways that results in paradoxical vasoconstrictive effects of H2S through inhibition of NO generation.

Indexed as

Vasodilation4-AminopyridineAlkynesAnimalsCells, CulturedCoronary VesselsCystathionine gamma-LyaseEndothelial CellsGlycineHemodynamicsHydrogen SulfideMiceNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide Synthase Type IIIPeptides4-AminopyridineAlkynesCystathionine gamma-LyaseGlycineHydrogen SulfideiberiotoxinNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide Synthase Type IIIPeptidesPotassium Channel Blockerspropargylglycinesodium sulfideSulfides

Identifiers

PMID24793048
OpenAlexW2092634836

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.