Evidence map›Paper›PMID 18414395›Full record

ArticleBritish journal of pharmacology2008

Oxidative stress and COX cause hyper-responsiveness in vascular smooth muscle of the femoral artery from diabetic rats.

Y Shi, P M Vanhoutte

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 88 citations in OpenAlex.

  1. Pathophysiology of homocysteine: insights into ion channel dysfunction.Pflugers Archiv : European journal of physiology · 2026
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  2. The machinery of healthy vasoconstriction: an overview.Pflugers Archiv : European journal of physiology · 2025
    Review
  3. Article
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  10. Redox Signaling and Regional Heterogeneity of Endothelial Dysfunction inInternational journal of molecular sciences · 2020
    Article
  11. Article
  12. Comparison of Pulmonary and Systemic NO- and PGIOxidative medicine and cellular longevity · 2018
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Flavonols in the Prevention of Diabetes-induced Vascular Dysfunction.Journal of cardiovascular pharmacology · 2015
    Review
  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

2 authors at 1 institution in 2 countries.

Y ShiDepartment of Pharmacology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China.
P M Vanhoutte
Chinese University of Hong Kong · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeTo investigate the dysfunction of vascular smooth muscle in streptozotocin-induced diabetic rats. EXPERIMENTAL APPROACH: Rings without endothelium of femoral arteries were suspended in organ chambers for isometric tension recording. The production of oxygen-derived free radicals was measured with 2',7'-dichlorodihydrofluorescein diacetate using confocal microscopy. The protein expressions were measured by western blotting. KEY

resultsThe concentration-response curves to U46619 and phenylephrine, but not that to KCl, were shifted to the left, suggesting a hypersensitivity of cell membrane receptors in diabetes. Exogenous oxygen-derived free radicals induced greater vasoconstrictions in the femoral artery from diabetic rats. Chronic treatment with apocynin (inhibitor of NADPH oxidase) and acute exposure to MnTMPyP (SOD/catalase mimetic) normalized the response. The catalase activity and the total glutathione level were reduced in arteries from streptozotocin-treated rats, confirming a redox abnormality. The basal oxidative state was higher in arteries from streptozotocin-treated rats and reduced in arteries from apocynin- and streptozotocin-treated rats, suggesting that the functional changes in diabetes are due to a chronic increase in oxidative stress. In the arteries of streptozotocin-treated rats, inhibitors of COX-1 and/or COX-2 prevented the hypersensitivity and reduced the increase in oxidative stress caused by phenylephrine and U46619, suggesting that both isoforms contribute to the smooth muscle dysfunction. The expression of proteins for COX-1 and COX-2 was increased in arteries of streptozotocin-treated rats and reduced in preparations of apocynin- and streptozotocin-treated rats. CONCLUSIONS AND IMPLICATIONS: Chronic diabetes and the resulting increased oxidative stress activate the production of COX-derived vasoconstrictor prostanoids causing hypersensitivity of vascular smooth muscle.

Indexed as

Oxidative StressAnimalsBlotting, WesternCyclooxygenase 1Cyclooxygenase 2Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Femoral ArteryFree RadicalsGene Expression RegulationMaleMuscle, Smooth, VascularNADPH OxidasesRatsRats, Sprague-DawleyStreptozocinCyclooxygenase 1Cyclooxygenase 2Free RadicalsNADPH OxidasesStreptozocin

Identifiers

PMID18414395
PMCPMC2439510
OpenAlexW2094145597

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.