Evidence map›Paper›PMID 10066940›Full record

ArticleThe Journal of physiology1999

In vitro simultaneous measurements of relaxation and nitric oxide concentration in rat superior mesenteric artery.

U Simonsen, R M Wadsworth, N H Buus, M J Mulvany

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.0field-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

35 citing papers in PubMed, 120 citations in OpenAlex.

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  11. Autoregulation and mechanotransduction control the arteriolar response to small changes in hematocrit.American journal of physiology. Heart and circulatory physiology · 2012
    Article
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  17. What is the real physiological NO concentration in vivo?Nitric oxide : biology and chemistry · 2009
    Review
  18. Inhibition of p38 MAPK reverses hypoxia-induced pulmonary artery endothelial dysfunction.American journal of physiology. Heart and circulatory physiology · 2009
    Article
  19. Article
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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

4 authors at 2 institutions in 2 countries.

U SimonsenDepartment of Pharmacology, University of Aarhus, 8000 Aarhus C, Denmark. us@farm.au.dk
R M Wadsworth
N H Buus
M J Mulvany
Aarhus University · DKUniversity of Strathclyde · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. The relationship between nitric oxide (NO) concentration measured with an NO-specific microelectrode and endothelium-dependent relaxation was investigated in isolated rat superior mesenteric artery contracted with 1 microM noradrenaline. 2. Acetylcholine (10 microM) induced endothelium-dependent simultaneous increases in luminal NO concentration of 21 +/- 6 nM, and relaxations with pD2 values and maximum of 6.95 +/- 0.32 and 97.5 +/- 0.7 % (n = 7), respectively. An inhibitor of NO synthase, N G-nitro-L-arginine (L-NOARG, 100 microM) inhibited the relaxations and increases in NO concentration induced by acetylcholine. 3. Oxyhaemoglobin (10 microM) reversed the relaxations and increases in NO concentrations induced by acetylcholine, S-nitroso-N-acetylpenicillamine (SNAP) and S-morpholino-sydnonimine (SIN-1), but not the relaxations induced with forskolin. Oxyhaemoglobin also decreased the NO concentration below baseline level. 4. In the presence of L-NOARG (100 microM), a small relaxation to acetylcholine (10 microM) of noradrenaline-contracted segments was still seen; oxyhaemogobin inhibited this relaxation and decreased the NO concentration by 14 +/- 4 nM (n = 4). 5. The NO concentration-relaxation relationship for acetylcholine resembled that for SNAP and SIN-1 more than for authentic NO. Thus while 7-17 nM NO induced half-maximal relaxations in response to SNAP or SIN-1, 378 +/- 129 nM NO (n = 4) was needed for half-maximal relaxation to authentic NO. 6. The present study provides direct evidence that the relaxation of the rat superior mesenteric artery with the endothelium-dependent vasodilator acetylcholine is correlated to the endogeneous release of NO. The study also suggests that NO mediates the L-NOARG-resistant relaxations in this artery, and that there is a basal NO release.

Indexed as

AcetylcholineAnimalsEndothelium, VascularEnzyme InhibitorsIn Vitro TechniquesMaleMesenteric Artery, SuperiorMicroelectrodesMolsidomineMuscle RelaxationMuscle, Smooth, VascularNitric OxideNitric Oxide DonorsNitric Oxide SynthaseNitric Oxide Synthase Type IIINitroarginineAcetylcholineEnzyme InhibitorslinsidomineMolsidomineNitric OxideNitric Oxide DonorsNitric Oxide SynthaseNitric Oxide Synthase Type IIINitroarginineNos3 protein, ratOxyhemoglobinsPenicillamineS-Nitroso-N-Acetylpenicillamine

Identifiers

PMID10066940
PMCPMC2269215
OpenAlexW1982993995

What OpenQuestion holds

Texttitle and abstract
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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.