Evidence map›Paper›PMID 10188968›Full record

ArticleBritish journal of pharmacology1999

Canine external carotid vasoconstriction to methysergide, ergotamine and dihydroergotamine: role of 5-HT1B/1D receptors and alpha2-adrenoceptors.

C M Villalón, P De Vries, G Rabelo, D Centurión, A Sánchez-López, P Saxena

Open access · bronzeAbstract read
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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-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

16 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. Ergot: from witchcraft to biotechnology.Molecular plant pathology · 2009
    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

6 authors at 2 institutions in 2 countries.

C M VillalónDepartamento de Farmacología y Toxicologia, CINVESTAV, I.P.N., México D.F., México. carlos_villalon@infosel.net.mx
P De Vries
G Rabelo
D Centurión
A Sánchez-López
P Saxena
Center for Research and Advanced Studies of the National Polytechnic Institute · MXErasmus University Rotterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The antimigraine drugs methysergide, ergotamine and dihydroergotamine (DHE) produce selective vasoconstriction in the external carotid bed of vagosympathectomized dogs anaesthetized with pentobarbital and artificially respired, but the receptors involved have not yet been completely characterized. Since the above drugs display affinity for several binding sites, including alpha-adrenoceptors and several 5-HT1 and 5-HT2 receptor subtypes, this study has analysed the mechanisms involved in the above responses. Intracarotid (i.c.) infusions during 1 min of methysergide (31-310 microg min(-1)), ergotamine (0.56-5.6 microg min(-1)) or DHE (5.6-31 microg min(-1)) dose-dependently reduced external carotid blood flow (ECBF) by up to 46+/-4, 37+/-4 and 49+/-5%, respectively. Blood pressure and heart rate remained unchanged. The reductions in ECBF by methysergide were abolished and even reversed to increases in animals pre-treated with GR127935 (10 microg kg(-1), i.v.). The reductions in ECBF by ergotamine and DHE remained unchanged in animals pre-treated (i.v.) with prazosin (300 microg kg(-1)), but were partly antagonized in animals pre-treated with either GR127935 (10 or 30 microg kg(-1)) or yohimbine (1000 microg kg(-1)). Pre-treatment with a combination of GR127935 (30 microg kg(-1)) and yohimbine (1000 microg kg(-1)) abolished the responses to both ergotamine and DHE. The above doses of antagonists were shown to produce selective antagonism at their respective receptors. These results suggest that the external carotid vasoconstrictor responses to methysergide primarily involve 5-HT1B/1D receptors, whereas those to ergotamine and DHE are mediated by 5-HT1B/1D receptors as well as alpha2-adrenoceptors.

Indexed as

Adrenergic alpha-1 Receptor AntagonistsAdrenergic alpha-2 Receptor AgonistsAdrenergic alpha-2 Receptor AntagonistsAdrenergic alpha-AgonistsAdrenergic alpha-AntagonistsAnimalsBlood Flow VelocityCarotid ArteriesClonidineDihydroergotamineDogsErgotamineFemaleHemodynamicsMaleMethysergideAdrenergic alpha-1 Receptor AntagonistsAdrenergic alpha-2 Receptor AgonistsAdrenergic alpha-2 Receptor AntagonistsAdrenergic alpha-AgonistsAdrenergic alpha-AntagonistsClonidineDihydroergotamineErgotamineGR 127935MethysergideOxadiazolesPhenylephrinePiperazinesPrazosinReceptors, Adrenergic, alpha-2Receptor, Serotonin, 5-HT1BReceptor, Serotonin, 5-HT1DReceptors, SerotoninSerotonin AntagonistsSumatriptanVasoconstrictor AgentsYohimbine

Identifiers

PMID10188968
PMCPMC1565835
OpenAlexW2118440775

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.