Evidence map›Paper›PMID 12684264›Full record

ArticleBritish journal of pharmacology2003

Mechanisms of hydrogen-peroxide-induced biphasic response in rat mesenteric artery.

Yu-Jing Gao, Simon Hirota, Da-Wei Zhang, Luke J Janssen, Robert M K W Lee

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2003. 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, 112 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Data Processing to Probe the Cellular Hydrogen Peroxide Landscape.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Oxidant Mechanisms in Renal Injury and Disease.Antioxidants & redox signaling · 2016
    Review
  12. Article
  13. Review
  14. Article
  15. Oxidative stress in hypertension: role of the kidney.Antioxidants & redox signaling · 2014
    Review
  16. Article
  17. Review
  18. Article
  19. 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

5 authors at 1 institution in 1 country.

Yu-Jing GaoDepartment of Anaesthesia, McMaster University, Hamilton, Ontario, Canada.
Simon Hirota
Da-Wei Zhang
Luke J Janssen
Robert M K W Lee
McMaster University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. In phenylephrine (PHE) (1 micro M)-precontracted superior mesenteric arteries from adult rats, low concentration of hydrogen peroxide (H(2)O(2), 10-100 micro M) caused only contraction, while high concentration of H(2)O(2) (0.3-1 mM) caused a biphasic response: a transient contraction followed by a relaxation response. 2. Endothelium removal did not affect the biphasic response. 7,7-Dimethyl-(5Z,8Z)-eicosadienoic acid, diclofenac, furegrelate, or SQ 29548 greatly inhibited the contraction but did not affect the relaxation. 17-Octadecynoic acid, eicosatriynoic acid, ICI 198615, SQ 22536, or ODQ did not inhibit the biphasic response. 3. KCl at 40 mM inhibited the relaxation response to H(2)O(2) by 98+/-24%. 4-Aminopyridine (4-AP) inhibited while tetraethylammonium chloride (TEA), charybdotoxin, or glibenclamide attenuated the relaxation response. A combination of 4-AP, TEA and glibenclamide mimicked the effects of 40 mM KCl. Iberiotoxin, apamin, or barium chloride did not inhibit the relaxation response. 4. H(2)O(2) at 1 mM hyperpolarized membrane potential and reversibly augmented K(+) current in smooth muscle cells of mesenteric artery. These effects of H(2)O(2) were attenuated significantly by 4-AP. 5. In summary, in PHE-precontracted rat mesenteric artery: (1) the response to H(2)O(2) shifted qualitatively from contraction to a biphasic response as H(2)O(2) increased to 0.3 mM or higher; (2) the relaxation response is caused by the activation of K(+) channels, with voltage-dependent K(+) channels playing a primary role; and the contraction is likely to be mediated by thromboxane A(2); (3) the K(+) channel activation by H(2)O(2) is independent of phospholipase A(2), cyclooxygenase, lipoxygenase, cytochrome P450 monooxygenase, adenylate or guanylate cyclase.

Indexed as

AnimalsDose-Response Relationship, DrugEnzyme InhibitorsHydrogen PeroxideMaleMesenteric ArteriesMuscle ContractionMuscle RelaxationMuscle, Smooth, VascularPhenylephrinePotassium Channel BlockersPotassium ChannelsRatsRats, Inbred WKYThromboxane A2Time FactorsEnzyme InhibitorsHydrogen PeroxidePhenylephrinePotassium Channel BlockersPotassium ChannelsThromboxane A2

Identifiers

PMID12684264
PMCPMC1573754
OpenAlexW2074664445

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.