Evidence map›Paper›PMID 11533140›Full record

ArticleThe Journal of physiology2001

Nitric oxide-cGMP pathway facilitates acetylcholine release and bradycardia during vagal nerve stimulation in the guinea-pig in vitro.

N Herring, D J Paterson

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In one paragraph

Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.

  1. Pooled it
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  11. Cardiac Sympathetic Denervation in Channelopathies.Frontiers in cardiovascular medicine · 2019
    Review
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  14. Cardiac sympatho-vagal balance and ventricular arrhythmia.Autonomic neuroscience : basic & clinical · 2016
    Review
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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

2 authors at 1 institution in 1 country.

N HerringUniversity Laboratory of Physiology, Parks Road, Oxford OX1 3PT, UK.
D J Paterson
University of Oxford · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

1. We tested the hypothesis that nitric oxide (NO) augments vagal neurotransmission and bradycardia via phosphorylation of presynaptic calcium channels to increase vesicular release of acetylcholine. 2. The effects of enzyme inhibitors and calcium channel blockers on the actions of the NO donor sodium nitroprusside (SNP) were evaluated in isolated guinea-pig atrial-right vagal nerve preparations. 3. SNP (10 microM) augmented the heart rate response to vagal nerve stimulation but not to the acetylcholine analogue carbamylcholine (100 nM). SNP also increased the release of [3H]acetylcholine in response to field stimulation. No effect of SNP was observed on either the release of [3H] acetylcholine or the HR response to vagal nerve stimulation in the presence of the guanylyl cyclase inhibitor 1H-(1,2,4)-oxadiazolo-(4,3-a)-quinoxalin-1-one (ODQ, 10 microM). 4. The phosphodiesterase 3 (PDE 3) inhibitor milrinone (1 microM) increased the release of [3H] acetylcholine and the vagal bradycardia and prevented any further increase by SNP. SNP was still able to augment the vagal bradycardia in the presence of the protein kinase G inhibitor KT5823 (1 microM) but not after protein kinase A (PKA) inhibition with H-89 (0.5 microM) or KT5720 (1 microM) had reduced the HR response to vagal nerve stimulation. Neither milrinone nor H-89 changed the HR response to carbamylcholine. 5. SNP had no effect on the magnitude of the vagal bradycardia after inhibition of N-type calcium channels with omega-conotoxin GVIA (100 nM). 6. These results suggests that NO acts presynaptically to facilitate vagal neurotransmission via a cGMP-PDE 3-dependent pathway leading to an increase in cAMP-PKA-dependent phosphorylation of presynaptic N-type calcium channels. This pathway may augment the HR response to vagal nerve stimulation by increasing presynaptic calcium influx and vesicular release of acetylcholine.

Indexed as

CarbazolesIndolesSulfonamidesAcetylcholineAlkaloidsAnimalsBradycardiaCalcium Channel BlockersCalcium ChannelsCarbacholCardiotonic AgentsCyclic AMP-Dependent Protein KinasesCyclic GMPElectric StimulationEnzyme InhibitorsFemale1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-oneAcetylcholineAlkaloidsCalcium Channel BlockersCalcium ChannelsCarbacholCarbazolesCardiotonic AgentsCyclic AMP-Dependent Protein KinasesCyclic GMPEnzyme InhibitorsGuanylate CyclaseIndolesIsoquinolinesKT 5823MilrinoneN-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamideNitric OxideNitric Oxide DonorsNitroprussideomega-Conotoxin GVIAOxadiazolesQuinoxalinesSulfonamidesTritium

Identifiers

PMID11533140
PMCPMC2278790
OpenAlexW2168278170

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.