Evidence map›Paper›PMID 20840539›Full record

ArticleBritish journal of pharmacology2011

Impairment of both nitric oxide-mediated and EDHF-type relaxation in small mesenteric arteries from rats with streptozotocin-induced diabetes.

C H Leo, J L Hart, O L Woodman

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
5.1field-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

61 citing papers in PubMed, 122 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. The Use of Wire Myography to Investigate Vascular Tone and Function.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Crocin Improves Endothelial Mitochondrial DysfunctionFrontiers in cell and developmental biology · 2021
    Article
  14. Antioxidant and Cytoprotective Effect of Quinoa (Antioxidants (Basel, Switzerland) · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

1 more citing papers are in PubMed but not listed here.

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.

C H LeoHealth Innovation Research Institute, RMIT University, Bundoora, Victoria, Australia.
J L Hart
O L Woodman
RMIT University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeTo investigate whether diabetes affects either or both nitric oxide (NO)-mediated and endothelium-derived hyperpolarizing factor (EDHF)-type relaxation in endothelium-dependent relaxation of mesenteric arteries from streptozotocin-induced diabetic rats. EXPERIMENTAL APPROACH: Wire myography was employed to examine endothelial function of mesenteric arteries. Superoxide levels were measured by L-012 and lucigenin-enhanced chemiluminescence. Western blotting was used to quantify protein expression levels. KEY

resultsSuperoxide levels were significantly increased in diabetic mesenteric arteries compared with normal arteries. Diabetes significantly reduced the sensitivity to the endothelium-dependent relaxant, acetylcholine (ACh) in mesenteric arteries. When the contribution of NO to relaxation was abolished by N-nitro-L-arginine (L-NNA) + a soluble guanylate cyclase inhibitor (ODQ), the sensitivity to ACh was significantly decreased in the diabetic arteries compared with normal arteries, indicating an impaired EDHF-type relaxation despite increased expression of intermediate- and small-conductance calcium-activated potassium channels. Conversely, when the contribution of EDHF was inhibited with TRAM-34 + apamin + iberiotoxin, maximum relaxations to ACh were significantly decreased in diabetic compared with normal arteries, suggesting that the contribution of NO was also impaired by diabetes. Basal levels of NO release, indicated by contraction to L-NNA, were also significantly decreased in diabetic arteries. Western blot analysis demonstrated that diabetic arteries had an increased expression of Nox2, decreased pSer⁴⁷³ Akt and a reduced proportion of endothelial NO synthase (eNOS) expressed as a dimer, indicating uncoupling. CONCLUSION AND IMPLICATIONS: The contribution of both NO and EDHF-type relaxations was impaired in diabetes and was caused by increased oxidative stress, decreased pSer⁴⁷³ Akt and/or eNOS uncoupling.

Indexed as

VasodilationAnimalsBiological FactorsBlood GlucoseBody WeightCyclooxygenase InhibitorsDiabetes Mellitus, ExperimentalEndothelium, VascularGlycated HemoglobinIndomethacinMaleMesenteric ArteriesNitric OxideOxidative StressRatsRats, Sprague-DawleyBiological FactorsBlood GlucoseCyclooxygenase Inhibitorsendothelium-dependent hyperpolarization factorGlycated Hemoglobinhemoglobin A1c protein, humanIndomethacinNitric OxideSmall-Conductance Calcium-Activated Potassium ChannelsSuperoxidesVasodilator Agents

Identifiers

PMID20840539
PMCPMC3031058
OpenAlexW1854619429

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.