Evidence map›Paper›PMID 10556946›Full record

ArticleBritish journal of pharmacology1999

Autoregulation of nitric oxide-soluble guanylate cyclase-cyclic GMP signalling in mouse thoracic aorta.

M B Hussain, A J Hobbs, R J MacAllister

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 64 citations in OpenAlex.

  1. Trial
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  6. Endothelium-specific amyloid precursor protein deficiency causes endothelial dysfunction in cerebral arteries.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
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  7. Review
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  16. Tonic and phasic nitric oxide signals in hippocampal long-term potentiation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006
    Article
  17. Article
  18. 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

3 authors at 1 institution in 1 country.

M B HussainWolfson Institute for Biomedical Research, University College London, The Rayne Institute, 5 University Street, London WC1E 6JJ, U.K.
A J Hobbs
R J MacAllister
University College London · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

1. The sensitivity of the soluble guanylate cyclase (sGC)-cyclic guanosine-3',5'-monophosphate (cyclic GMP) system to nitric oxide (NO) was investigated in mouse aorta from wild type (WT) and NO synthase (NOS) knockout (KO) animals. 2. The NO donor, spermine-NONOate (SPER-NO) was more potent in aortas from eNOS KO mice compared to WT (pEC50 7.30+/-0.06 and 6.56+/-0.04, respectively; n=6; P<0.05). In contrast, the non-NO based sGC activator, YC-1 was equipotent in vessels from eNOS WT and KO mice. The sensitivity of aortas from nNOS and iNOS KO animals to SPER-NO was unchanged. Forskolin (an adenylate cyclase activator), was equipotent in vessels from eNOS WT and KO animals. 3. The cyclic GMP analogue, 8-Br-cGMP was equipotent in eNOS WT and KO mice (pEC50 4. 38+/-0.04 and 4.40+/-0.05, respectively; n=5; P>0.05). Zaprinast (10-5 M) a phosphodiesterase type V (PDE V) inhibitor, had no effect on the response to SPER-NO in vessels from eNOS WT or KO mice. 4. The NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 3x10-4 M) increased the potency of SPER-NO in aortas from WT mice (pEC50 6. 64+/-0.02 and 7.37+/-0.02 in the absence and presence of L-NAME, respectively; n=4; P<0.05). 5. In summary, there is increased sensitivity of vessels from eNOS KO animals to NO. Cyclic AMP-mediated dilatation is unchanged, consistent with a specific up-regulation of sGC - cyclic GMP signalling. The functional activity of cyclic GMP-dependent protein kinase (G-kinase) and PDE V was also unchanged, suggesting that sGC is the site of up-regulation. These alterations in the sensitivity of the sGC - cyclic GMP pathway might represent a mechanism for the dynamic regulation of NO bioactivity.

Indexed as

3',5'-Cyclic-GMP Phosphodiesterases8-Bromo Cyclic Adenosine MonophosphateAnimalsAorta, ThoracicColforsinCyclic GMPCyclic Nucleotide Phosphodiesterases, Type 5Guanylate CyclaseHomeostasisIndazolesMaleMiceMice, Inbred C57BLMice, KnockoutNitric OxideNitric Oxide Synthase3',5'-Cyclic-GMP Phosphodiesterases3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole8-Bromo Cyclic Adenosine MonophosphateColforsinCyclic GMPCyclic Nucleotide Phosphodiesterases, Type 5Guanylate CyclaseIndazolesNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINitrogen OxidesNos2 protein, mouseNos3 protein, mousePde5a protein, mousePhosphodiesterase InhibitorsPhosphoric Diester HydrolasesPlatelet Aggregation InhibitorsPurinonesSperminespermine nitric oxide complexzaprinast

Identifiers

PMID10556946
PMCPMC1571718
OpenAlexW2006958729

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.