Evidence map›Paper›PMID 18790700›Full record

ArticleLife sciences2008

Hydrogen sulfide decreases adenosine triphosphate levels in aortic rings and leads to vasorelaxation via metabolic inhibition.

Levente Kiss, Edwin A Deitch, Csaba Szabó

Abstract read
In one paragraph

Article in Life sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
7.6field-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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Homocysteine Attack on Vascular Endothelium-Old and New Features.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Hydrogen sulfide and its role in female reproduction.Frontiers in veterinary science · 2024
    Review
  9. Review
  10. Comparative Study of Different HAntioxidants (Basel, Switzerland) · 2023
    Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. The Cardiovascular Effects of Hydrogen Sulfide: The Epigenetic Mechanisms.Advances in experimental medicine and biology · 2021
    Article
  16. Review
  17. Review
  18. Review
  19. Hydrogen sulfide, oxygen, and calcium regulation in developing human airway smooth muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  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

3 authors at 2 institutions in 1 country.

Levente KissDepartment of Surgery, University of Medicine and Dentistry of New Jersey, 185 South Orange Avenue, University Heights, Newark, NJ 07103-2714, USA.
Edwin A Deitch
Csaba Szabó
Rutgers, The State University of New Jersey · USThe University of Texas Medical Branch at Galveston · US

Funding

POLY (ADP RIBOSE) SYNTHETASE AND PEROXYNITRITE INDUCED CR01GM060915 · NIGMS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SZABO, CSABA · 1999 to 2009
$1.9M
NIGMS NIH HHS R01 GM060915
6 · The paper itself

Abstract

aimsHydrogen sulfide (H(2)S) at low concentrations serves as a physiological endogenous vasodilator molecule, while at higher concentrations it can trigger cytotoxic effects. The aim of our study was to elucidate the potential mechanisms responsible for the effects of H(2)S on vascular tone. MAIN

methodsWe measured the vascular tone in vitro in precontracted rat thoracic aortic rings and we have tested the effect of different oxygen levels and a variety of inhibitors affecting known vasodilatory pathways. We have also compared the vascular effect of high concentrations of H(2)S to those of pharmacological inhibitors of oxidative phosphorylation. Furthermore, we measured adenosine triphosphate (ATP)-levels in the same vascular tissues. KEY

findingsWe have found that in rat aortic rings: (1) H(2)S decreases ATP levels; (2) relaxations to H(2)S depend on the ambient oxygen concentration; (3) prostaglandins do not take part in the H(2)S induced relaxations; (4) the 3':5'-cyclic guanosine monophosphate (cGMP)-nitric oxide (NO) pathway does not have a role in the relaxations (5) the role of K(ATP) channels is limited, while Cl(-)/HCO(3)(-) channels have a role in the relaxations. (6): We have observed that high concentrations of H(2)S relax the aortic rings in a fashion similar to sodium cyanide, and both agents reduce cellular ATP levels to a comparable degree. SIGNIFICANCE: H(2)S, a new gasotransmitter of emerging importance, leads to relaxation via Cl(-)/HCO(3)(-) channels and metabolic inhibition and the interactions of these two factors depend on the oxygen levels of the tissue.

Indexed as

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic AcidAdenosine TriphosphateAnimalsAorta, ThoracicDose-Response Relationship, DrugGlyburideHydrogen SulfideKATP ChannelsMaleNitric OxideOxidative PhosphorylationProstaglandinsRatsRats, WistarVasodilation4,4'-Diisothiocyanostilbene-2,2'-Disulfonic AcidAdenosine TriphosphateGlyburideHydrogen SulfideKATP ChannelsNitric OxideProstaglandins

Identifiers

PMID18790700
PMCPMC4225123
OpenAlexW2061049180

What OpenQuestion holds

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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.