Evidence map›Paper›PMID 8751089›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology1995

Functional serotonin 5-HT1D receptors and 5-HT1D beta receptor mRNA expression in human umbilical vein endothelial cells.

P Schoeffter, C Ullmer, M Gutierrez, G Weitz-Schmidt, H Lübbert

Abstract read
PubMed Publisher
In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 47% 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

5 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. 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

5 authors at 1 institution in 1 country.

P SchoeffterSandoz Pharma Ltd, Basel, Switzerland.
C Ullmer
M Gutierrez
G Weitz-Schmidt
H Lübbert
Sanden (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pharmacological evidence has suggested the presence of 5-hydroxytryptamine (5-HT, serotonin), 5-HT(1D) receptors on endothelial cells but these receptors have never been identified unambiguously on this type of cells. We now report that human umbilical vein endothelial cells (HUVEC) express 5-HT(1D) receptors coupled to inhibition of cyclic AMP formation. 5-HT and 5-HT(1D) receptor agonists 5-carboxamidotryptamine (5-CT) and sumatriptan were approximately equipotent at inhibiting forskolin-stimulated cyclic AMP accumulation in HUVEC (mean pEC50 7.6-8.2, maximal effect 30% inhibition). The 5-HT(1A) receptor antagonist, 8-OH-DPAT was clearly less potent (pEC50 6.2) and less efficacious. The selective 5-HT(1D) receptor agonist, GR127935 (1 nM) markedly inhibited the effect of 5-HT (apparent pK(B) 10.8). Reverse transcription-polymerase chain reaction analysis showed the mRNA for 5-HT(1D beta) receptors to be expressed in HUVEC. These results demonstrate the presence of functional 5-HT(1D) receptors and the expression of 5-HT(1D beta) receptor mRNA in HUVEC. They support the involvement of 5-HT(1D beta) receptors in endothelial-mediated responses to 5-HT.

Indexed as

8-Hydroxy-2-(di-n-propylamino)tetralinCells, CulturedColforsinCyclic AMPEndothelium, VascularHumansPolymerase Chain ReactionReceptors, SerotoninRNA, MessengerSerotoninSerotonin AntagonistsSerotonin Receptor AgonistsSumatriptanUmbilical Veins5-carboxamidotryptamine8-Hydroxy-2-(di-n-propylamino)tetralinColforsinCyclic AMPReceptors, SerotoninRNA, MessengerSerotoninSerotonin AntagonistsSerotonin Receptor AgonistsSumatriptan

Identifiers

PMID8751089
OpenAlexW2003353488

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.