Evidence map›Paper›PMID 23117109›Full record

ArticleVascular pharmacology2013

Signal transduction and modulating pathways in tryptamine-evoked vasopressor responses of the rat isolated perfused mesenteric bed.

M Akhtar Anwar, William R Ford, Amy A Herbert, Kenneth J Broadley

Open access · hybridAbstract read
In one paragraph

Article in Vascular pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Frontiers in pharmacology · 2018
    Article
  7. Article
  8. Pathogenesis of chronic cluster headache and bouts: role of tryptamine, arginine metabolism and αNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017
    Article
  9. Article
  10. Biochemistry of primary headaches: role of tyrosine and tryptophan metabolism.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2015
    Review
  11. Tryptamine levels are low in plasma of chronic migraine and chronic tension-type headache.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2014
    Article
  12. Perivascular adipose tissue contains functional catecholamines.Pharmacology research & perspectives · 2014
    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

4 authors at 1 institution in 1 country.

M Akhtar AnwarDivision of Pharmacology, Cardiff School of Pharmacy & Pharmaceutical Sciences, Cardiff University, Cathays Park, Cardiff CF10 3NB, UK.
William R Ford
Amy A Herbert
Kenneth J Broadley
Cardiff University · GB

Funding

British Heart Foundation PG/09/021British Heart Foundation PG/09/021/26544Wellcome TrustWellcome Trust 069301/Z/02/Z
6 · The paper itself

Abstract

Tryptamine is an endogenous and dietary indoleamine-based trace amine implicated in cardiovascular pathologies, including hypertension, migraine and myocardial infarction. This study aimed at identifying the signalling pathways for the vasoconstrictor response to tryptamine in rat isolated perfused mesenteric arterial beds and co-released vasodilator modulators of tryptamine-mediated vasoconstriction. Tryptamine caused concentration-dependent vasoconstriction of the mesenteric bed, measured as increases in perfusion pressure. These were inhibited by the 5-HT(2A) receptor antagonist, ritanserin, indicating mediation via 5-HT(2A) receptors. The response was inhibited by the phospholipase C (PLC) and phospholipase A(2) (iPLA(2)) inhibitors, U-73122 and PACOCF(3), suggesting involvement of phospholipase pathways. Activation of these pathways by tryptamine releases cyclooxygenase (COX) products since indomethacin (non-selective inhibitor of COX-1/2) and nimesulide (selective COX-2 inhibitor) reduced the vasoconstriction. The most likely COX vasoconstrictor product was prostaglandin PGE(2) since the responses to tryptamine were reduced by AH-6809, a non-selective EP(1) receptor antagonist. Involvement of the Rho-kinase pathway in the tryptamine-evoked vasoconstriction was also indicated by its reduction by the Rho-kinase inhibitors, Y-27,632 and fasudil. The tryptamine vasoconstriction is modulated by the co-released endothelial vasodilator, nitric oxide. Thus, circulating tryptamine can regulate mesenteric blood flow through a cascade of signalling pathways secondary to stimulation of 5-HT(2A) receptors.

Indexed as

AnimalsDinoprostoneDose-Response Relationship, DrugMaleMesenteric ArteriesNitric OxideRatsRats, Sprague-DawleyReceptor, Serotonin, 5-HT2Arho-Associated KinasesRitanserinSerotonin 5-HT2 Receptor AntagonistsSignal TransductionTryptaminesVasoconstrictionVasodilationDinoprostoneNitric OxideReceptor, Serotonin, 5-HT2Arho-Associated KinasesRitanserinSerotonin 5-HT2 Receptor AntagoniststryptamineTryptamines

Identifiers

PMID23117109
PMCPMC3884126
OpenAlexW2042116981

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.