Evidence map›Paper›PMID 11139458›Full record

ArticleBritish journal of pharmacology2000

Local regulation of [(3)H]-noradrenaline release from the isolated guinea-pig right atrium by P(2X)-receptors located on axon terminals.

B Sperlágh, F Erdélyi, G Szabó, E S Vizi

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Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 45 citations in OpenAlex.

  1. A cyclic pathway of P2 × 7, bradykinin, and dopamine receptor activation induces a sustained articular hyperalgesia in the knee joint of rats.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
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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 3 institutions in 2 countries.

B SperlághDepartment of Pharmacology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, H-1450 Budapest, POB 67, Hungary.
F Erdélyi
G Szabó
E S Vizi
Hungarian Academy of Sciences · HUHUN-REN Institute of Experimental Medicine · HUMRC Laboratory of Molecular Biology · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study the regulation of cardiac sympathetic outflow by presynaptic P(2X) receptor-gated ion channels was examined. ATP (30 microM - 1 mM) and other P2-receptor agonists elicited [(3)H]-noradrenaline ([(3)H]-NA) outflow from the isolated guinea-pig right atrium with the potency order of ATP>2-methyl-thioATP>alpha,beta-methylene-ATP=ADP, whereas ss, gamma-methylene-L-ATP was inactive. Ca(2+)-free conditions abolished both electrical field stimulation (EFS)- and ATP-evoked release of tritium. Unlike from EFS-induced outflow, ATP-induced [(3)H]-NA outflow was not reduced by omega-Conotoxin-GVIA (100 nM), Cd(2+) (100 microM) and tetrodotoxin (1 microM). The rapid extracellular decomposition of ATP was revealed by HPLC analysis. However, the effect of ATP to promote [(3)H]-NA release was not prevented by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 250 nM), 3, 7-dimethyl-1-propargylxanthine (DMPX, 250 nM), or by reactive blue 2 (RB2, 10 microM), antagonists of A(1)-, A(2)- and inhibitory P(2) receptors. Zn(2+) (50 microM), the P(2X)-receptor modulator potentiated, and P(2X) receptor antagonists, i.e. suramin (300 microM), pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 30 microM) and 2'-o-(trinitrophenyl)-adenosine 5'-triphosphate (TNP-ATP, 30 microM) antagonized the ATP (1 mM)-evoked response. RT - PCR study revealed the expression of P(2X2) and P(2X3) receptor mRNAs in guinea-pig superior cervical ganglion. PPADS (30 microM) significantly reduced the EFS-induced [(3)H]-NA outflow in the presence DPCPX (250 nM) and RB2 (10 microM). In summary a P(2X)-type purinoceptor regulates noradrenaline release from the isolated right atrium of the guinea-pig. The pharmacological profile of the receptor resemble to homo-oligomeric P(2X3) or hetero-oligomeric P(2X2)/P(2X3) complexes, and provide a new target to intervene on sympathetic neuroeffector transmission at the presynaptic site.

Indexed as

Adenosine DiphosphateAdenosine TriphosphateAnimalsCadmiumDose-Response Relationship, DrugElectric StimulationGene ExpressionGuinea PigsHeart AtriaHippocampusIn Vitro TechniquesMaleNorepinephrineomega-Conotoxin GVIAPresynaptic TerminalsPurinergic P2 Receptor Agonists1,3-dipropyl-8-cyclopentylxanthine2-methylthio-ATP3,7-dimethyl-1-propargylxanthine5'-adenylyl (beta,gamma-methylene)diphosphonateAdenosine DiphosphateAdenosine Triphosphatealpha,beta-methyleneadenosine 5'-triphosphateCadmiumNorepinephrineomega-Conotoxin GVIAPurinergic P2 Receptor AgonistsPurinergic P2 Receptor AntagonistsPyridoxal Phosphatepyridoxal phosphate-6-azophenyl-2',4'-disulfonic acidReceptors, Purinergic P2RNATetrodotoxinTheobromineThionucleotidesTritiumXanthines

Identifiers

PMID11139458
PMCPMC1572515
OpenAlexW2069502793

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.