Evidence map›Paper›PMID 10639106›Full record

ArticleThe Journal of physiology2000

Inhibition of nitric oxide synthase augments the positive inotropic effect of nitric oxide donors in the rat heart.

G Müller-Strahl, K Kottenberg, H G Zimmer, E Noack, G Kojda

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Phosphodiesterases: Evolving Concepts and Implications for Human Therapeutics.Annual review of pharmacology and toxicology · 2025
    Review
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  7. Nitric oxide: a new role in intensive care.Critical care and resuscitation : journal of the Australasian Academy of Critical Care Medicine · 2020
    Article
  8. Article
  9. Article
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  11. Article
  12. Article
  13. Article
  14. Nitric oxide control of cardiac function: is neuronal nitric oxide synthase a key component?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2004
    Review
  15. Article
  16. Review
  17. Myocardial dysfunction in sepsis: no role for NO?Heart (British Cardiac Society) · 2002
    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

5 authors at 2 institutions in 1 country.

G Müller-StrahlInstitut für Pharmakologie und Klinische Pharmakologie, Medizinische Einrichtungen, Heinrich-Heine-Universitat, 40225 Dusseldorf and Carl-Ludwig-Institut fur Physiologie, G.M.-S., H.-G.Z., Universität Leipzig, Liebigstrasse 27, 04103 Leipzig, Germ.
K Kottenberg
H G Zimmer
E Noack
G Kojda
Leipzig University · DEHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. In this investigation we studied the effects of nitric oxide on contractility and heart rate in normal saline-perfused rat hearts where shear stress-induced endothelial NO synthesis substantially contributes to total cardiac NO production. In addition, we sought to estimate the concentrations of exogenous NO producing inotropic effects. 2. We investigated the effects of glyceryl trinitrate (GTN), S-nitroso-d,l-penicillamine (SNAP), sodium (Z)-1-(N, N-diethylamino)diazen-1-ium-1,2-diolat (DEA/NO), and DEA/NO in the presence of the NO synthase inhibitor Nomega-nitro-L-arginine (L-NA) in constant-flow-perfused spontaneously beating rat Langendorff hearts and in rat working hearts. 3. In Langendorff hearts, GTN (10 nM to 100 microM, n = 32) induced a positive inotropic response that plateaued at 1 microM GTN with a maximal rate of increase of left ventricular pressure during ventricular contraction (+dP/dtmax) of 6. 33 +/- 2.56 % (n = 11, P < 0.5). Similarly, both spontaneous NO donors (0.1 nM to 1 microM, corresponding to approximately 0.03-0.3 microM NO) induced a positive inotropic response of 10.6 +/- 3.1 % (SNAP; n = 15, P < 0.05) and 11.5 +/- 2.7 % (DEA/NO, n = 15, P < 0. 05). 4. The positive inotropic effect of SNAP and DEA/NO progressively declined from 1 microM to 100 microM of the NO donors (corresponding to approximately 0.3-30 microM NO). 5. In the isolated working rat heart, 0.1 microM DEA/NO induced an increase of +dP/dtmax of 7.5 +/- 2.5 % (n = 9, P < 0.05). Inhibition of NO synthase by L-NA produced a 4-fold increase in this effect of DEA/NO. 6. We suggest that physiological NO concentrations support myocardial performance. In normal rat hearts the positive inotropic effect of NO appears to be almost maximally exploited by the endogenous NO production.

Indexed as

AnimalsCardiotonic AgentsDrug SynergismEnzyme InhibitorsFemaleHeartHydrazinesIn Vitro TechniquesMaleMyocardial ContractionMyocardiumNitric Oxide DonorsNitric Oxide SynthaseNitric Oxide Synthase Type IIINitroarginineNitrogen Oxides1,1-diethyl-2-hydroxy-2-nitrosohydrazineCardiotonic AgentsEnzyme InhibitorsHydrazinesNitric Oxide DonorsNitric Oxide SynthaseNitric Oxide Synthase Type IIINitroarginineNitrogen OxidesNitroglycerinNos3 protein, ratPenicillamineS-Nitroso-N-AcetylpenicillamineVasodilator Agents

Identifiers

PMID10639106
PMCPMC2269760
OpenAlexW1969309351

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.