Evidence map›Paper›PMID 23349456›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2013

Pharmacological inhibition of S-nitrosoglutathione reductase improves endothelial vasodilatory function in rats in vivo.

Qiumei Chen, Richard E Sievers, Monika Varga, Sourabh Kharait, Daniel J Haddad, Aaron K Patton, Christopher S Delany, Sarah C Mutka, Joan P Blonder, Gregory P Dubé and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Bronchopulmonary Dysplasia and Pulmonary Hypertension. The Role of Smooth MuscleAmerican journal of respiratory cell and molecular biology · 2021
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Infection and immunity · 2017
    Article
  15. Review
  16. Review
  17. Article
  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

12 authors at 3 institutions in 1 country.

Qiumei ChenCardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94143-0124, USA.
Richard E Sievers
Monika Varga
Sourabh Kharait
Daniel J Haddad
Aaron K Patton
Christopher S Delany
Sarah C Mutka
Joan P Blonder
Gregory P Dubé
Gary J Rosenthal
Matthew L Springer
Nivalis Therapeutics (United States) · USUniversity of California, San Francisco · USBroad Center · US

Funding

Academic Training Program in NephrologyT32DK007219 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HSU, CHI-YUAN · 1986 to 2022
$7.3M
The Role of Nitric Oxide Synthase in Circulating Progenitor Cell FunctionR01HL086917 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SPRINGER, MATTHEW LAWRENCE · 2007 to 2011
$2.1M
NHLBI NIH HHS R01 HL-086917NIDDK NIH HHS T32 DK007219
6 · The paper itself

Abstract

Nitric oxide (NO) exerts a wide range of cellular effects in the cardiovascular system. NO is short lived, but S-nitrosoglutathione (GSNO) functions as a stable intracellular bioavailable NO pool. Accordingly, increased levels can facilitate NO-mediated processes, and conversely, catabolism of GSNO by the regulatory enzyme GSNO reductase (GSNOR) can impair these processes. Because dysregulated GSNOR can interfere with processes relevant to cardiovascular health, it follows that inhibition of GSNOR may be beneficial. However, the effect of GSNOR inhibition on vascular activity is unknown. To study the effects of GSNOR inhibition on endothelial function, we treated rats with a small-molecule inhibitor of GSNOR (N6338) that has vasodilatory effects on isolated aortic rings and assessed effects on arterial flow-mediated dilation (FMD), an NO-dependent process. GSNOR inhibition with a single intravenous dose of N6338 preserved FMD (15.3 ± 5.4 vs. 14.2 ± 6.3%, P = nonsignificant) under partial NO synthase inhibition that normally reduces FMD by roughly 50% (14.1 ± 2.9 vs. 7.6 ± 4.4%, P < 0.05). In hypertensive rats, daily oral administration of N6338 for 14 days reduced blood pressure (170.0 ± 5.3/122.7 ± 6.4 vs. 203.8 ± 1.9/143.7 ± 7.5 mmHg for vehicle, P < 0.001) and vascular resistance index (1.5 ± 0.4 vs. 3.2 ± 1.0 mmHg · min · l(-1) for vehicle, P < 0.001), and restored FMD from an initially impaired state (7.4 ± 1.7%, day 0) to a level (13.0 ± 3.1%, day 14, P < 0.001) similar to that observed in normotensive rats. N6338 also reversed the pathological kidney changes exhibited by the hypertensive rats. GSNOR inhibition preserves FMD under conditions of impaired NO production and protects against both microvascular and conduit artery dysfunction in a model of hypertension.

Indexed as

Administration, OralAldehyde OxidoreductasesAnimalsAntihypertensive AgentsBlood PressureCells, CulturedDisease Models, AnimalDose-Response Relationship, DrugEndothelium, VascularEnzyme InhibitorsFemoral ArteryHumansHypertensionInjections, IntravenousKidneyMiceAldehyde OxidoreductasesAntihypertensive AgentsEnzyme Inhibitorsformaldehyde dehydrogenase, glutathione-independentNitric OxideNitric Oxide Synthase Type IIINos3 protein, ratSodium Chloride, DietaryVasodilator Agents

Identifiers

PMID23349456
PMCPMC3615603
OpenAlexW2124906369

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.