Evidence map›Paper›PMID 26236485›Full record

ArticlePharmacology research & perspectives2015

Pharmacological profiling of the hemodynamic effects of cannabinoid ligands: a combined in vitro and in vivo approach.

Sarah K Walsh, Claire Y Hepburn, Oliver Keown, Annika Åstrand, Anna Lindblom, Erik Ryberg, Stephan Hjorth, Stephan J Leslie, Peter J Greasley, Cherry L Wainwright

Open access · goldAbstract read
In one paragraph

Article in Pharmacology research & perspectives, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.8field-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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  6. CBInternational journal of molecular sciences · 2020
    Article
  7. Targeting CBMolecular neurobiology · 2019
    Article
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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

10 authors at 3 institutions in 2 countries.

Sarah K WalshInstitute for Health & Wellbeing Research, Robert Gordon University Riverside East, Aberdeen, AB10 7GJ, United Kingdom.
Claire Y HepburnInstitute for Health & Wellbeing Research, Robert Gordon University Riverside East, Aberdeen, AB10 7GJ, United Kingdom.
Oliver KeownInstitute for Health & Wellbeing Research, Robert Gordon University Riverside East, Aberdeen, AB10 7GJ, United Kingdom ; Cardiac Unit, Raigmore Hospital Old Perth Road, Inverness, IV2 3UJ, United Kingdom.
Annika ÅstrandCardiovascular & Metabolic Disease IMED, AstraZeneca R&D Mölndal, Sweden.
Anna LindblomCardiovascular & Metabolic Disease IMED, AstraZeneca R&D Mölndal, Sweden.
Erik RybergCardiovascular & Metabolic Disease IMED, AstraZeneca R&D Mölndal, Sweden.
Stephan HjorthCardiovascular & Metabolic Disease IMED, AstraZeneca R&D Mölndal, Sweden.
Stephan J LeslieCardiac Unit, Raigmore Hospital Old Perth Road, Inverness, IV2 3UJ, United Kingdom.
Peter J GreasleyCardiovascular & Metabolic Disease IMED, AstraZeneca R&D Mölndal, Sweden.
Cherry L WainwrightInstitute for Health & Wellbeing Research, Robert Gordon University Riverside East, Aberdeen, AB10 7GJ, United Kingdom.
AstraZeneca (Sweden) · SERobert Gordon University · GBRaigmore Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The receptors mediating the hemodynamic responses to cannabinoids are not clearly defined due to the multifarious pharmacology of many commonly used cannabinoid ligands. While both CB1 and TRPV1 receptors are implicated, G protein-coupled receptor 55 (GPR55) may also mediate some of the hemodynamic effects of several atypical cannabinoid ligands. The present studies attempted to unravel the pharmacology underlying the in vivo hemodynamic responses to ACEA (CB1 agonist), O-1602 (GPR55 agonist), AM251 (CB1 antagonist), and cannabidiol (CBD; GPR55 antagonist). Agonist and antagonist profiles of each ligand were determined by ligand-induced GTPγS binding in membrane preparations expressing rat and mouse CB1 and GPR55 receptors. Blood pressure responses to ACEA and O-1602 were recorded in anesthetized and conscious mice (wild type, CB1 (-/-) and GPR55(-/-)) and rats in the absence and presence of AM251 and CBD. ACEA demonstrated GTPγS activation at both receptors, while O-1602 only activated GPR55. AM251 exhibited antagonist activity at CB1 and agonist activity at GPR55, while CBD demonstrated selective antagonist activity at GPR55. The depressor response to ACEA was blocked by AM251 and attenuated by CBD, while O-1602 did not induce a depressor response. AM251 caused a depressor response that was absent in GPR55(-/-) mice but enhanced by CBD, while CBD caused a small vasodepressor response that persisted in GPR55(-/-) mice. Our findings show that assessment of the pharmacological profile of receptor activation by cannabinoid ligands in in vitro studies alongside in vivo functional studies is essential to understand the role of cannabinoids in hemodynamic control.

Indexed as

CannabinoidsCB1 receptorG protein coupled receptor 55hemodynamics

Identifiers

PMID26236485
PMCPMC4492759
OpenAlexW1927830536

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.