Evidence map›Paper›PMID 12719994›Full record

ArticleGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2003

Elevation of nitric oxide production in human trabecular meshwork by increased pressure.

Andrea Schneemann, Ateunette Leusink-Muis, Thomas van den Berg, Philip F J Hoyng, Willem Kamphuis

Abstract read
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In one paragraph

Article in Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact, top 81% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

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  15. Article
  16. The nitric oxide-guanylate cyclase pathway and glaucoma.Nitric oxide : biology and chemistry · 2018
    Review
  17. Article
  18. Role of nitric oxide in murine conventional outflow physiology.American journal of physiology. Cell physiology · 2015
    Article
  19. Review
  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 3 institutions in 1 country.

Andrea SchneemannGlaucoma Research Group, Netherlands Ophthalmic Research Institute, KNAW, Meibergdreef 47, 1105 BA Amsterdam, The Netherlands.
Ateunette Leusink-Muis
Thomas van den Berg
Philip F J Hoyng
Willem Kamphuis
Combined Ophthalmic Research Rotterdam · NLNetherlands Institute for Neuroscience · NLUtrecht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe presence of the nitric oxide (NO)-producing enzyme nitric oxide synthase (NOS) in the trabecular meshwork and the effect of various drugs acting through the NO pathway on the outflow facility and trabecular contractility suggest a role for NO in the regulation of outflow and intraocular pressure (IOP).

methodsTo model the effect of elevated IOP on the NO production in the trabecular meshwork, we perfused anterior segments of human donor eyes in vitro and studied the effect of raised perfusion pressure on NO levels in the perfusate. Furthermore, we evaluated using quantitative PCR whether enhanced perfusion pressure had an effect on the NOS gene expression levels.

resultsElevating the pressure from 10 mmHg to 25 mmHg caused a significant increase in NO production from 3.6+/-0.9 pmol/min to 5.9+/-1.6 pmol/min (mean +/- SEM), corresponding to an average increase of 66%. These high NO levels were reduced by application of L-NAME, an NOS inhibitor, to 2.6+/-0.6 pmol/min. Addition of L-NAME before raising the pressure decreased the basal NO production but was not able to block the increase in NO production after raising the pressure. The transcript level of iNOS was significantly increased in the trabecular meshwork after raising the perfusion pressure.

conclusionThese results show that NO production increased after elevation of the pressure gradient over the trabecular meshwork, accompanied by an upregulation of iNOS gene expression. Previous studies have demonstrated that enhanced NO levels facilitate outflow. Taken together, the data indicate the existence of a regulatory feedback mechanism in the trabecular meshwork, which may contribute to the regulation of the IOP. In this system an increase in IOP will enhance NO production, which, in turn, increases the outflow facility, leading to a normalization of the IOP.

Indexed as

AgedAnterior Eye SegmentEnzyme InhibitorsHumansIntraocular PressureNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IIOcular HypertensionPolymerase Chain ReactionPressureRNA, MessengerTrabecular MeshworkUp-RegulationEnzyme InhibitorsNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IINOS2 protein, humanRNA, Messenger

Identifiers

PMID12719994
OpenAlexW2057554731

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.