ArticleBritish journal of pharmacology2007
The novel endocannabinoid receptor GPR55 is activated by atypical cannabinoids but does not mediate their vasodilator effects.
Article in British journal of pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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Who cites it
104 citing papers in PubMed, 241 citations in OpenAlex.
- The Potential of Cannabidiol for the Treatment of Psychosis: Endocannabinoid Regulation of Serotonergic Neurotransmission via Serotonin 5-HT1A/2A Receptors.Neurochemical research · 2026Review
- Exacerbated cardiac dysfunction from combined alcohol binge and synthetic cannabinoid use.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Structural basis for lipid-mediated activation of G protein-coupled receptor GPR55.Nature communications · 2025Article
- Cannabidiol improves learning and memory deficits and alleviates anxiety in 12-month-old SAMP8 mice.PloS one · 2025Article
- GPR55 Antagonist CID16020046 Attenuates Obesity-Induced Airway Inflammation by Suppressing Chronic Low-Grade Inflammation in the Lungs.International journal of molecular sciences · 2024Article
- Synthesis of Neocannabinoids Using Controlled Friedel-Crafts Reactions.The Journal of organic chemistry · 2023Article
- Therapeutic Effects of Cannabinoids and Their Applications in COVID-19 Treatment.Life (Basel, Switzerland) · 2022Review
- Lysophosphatidylinositol Induced Morphological Changes and Stress Fiber Formation through the GPR55-RhoA-ROCK Pathway.International journal of molecular sciences · 2022Article
- Novel Noninvasive Approaches to the Treatment of Obesity: From Pharmacotherapy to Gene Therapy.Endocrine reviews · 2022Review
- Acute and long-term effects of cannabinoids on hypertension and kidney injury.Scientific reports · 2022Article
- GPR55 Antagonist CID16020046 Protects against Atherosclerosis Development in Mice by Inhibiting Monocyte Adhesion and Mac-1 Expression.International journal of molecular sciences · 2021Article
- Endocannabinoid signaling pathways: beyond CB1R and CB2R.Journal of cell communication and signaling · 2021Review
- GPR119 and GPR55 as Receptors for Fatty Acid Ethanolamides, Oleoylethanolamide and Palmitoylethanolamide.International journal of molecular sciences · 2021Review
- Synthetic and Natural Derivatives of Cannabidiol.Advances in experimental medicine and biology · 2021Article
- The Essential Medicinal Chemistry of Cannabidiol (CBD).Journal of medicinal chemistry · 2020Review
- Juniperonic Acid Biosynthesis is Essential inCells · 2020Article
- The Effects of Cannabidiol, a Non-Intoxicating Compound of Cannabis, on the Cardiovascular System in Health and Disease.International journal of molecular sciences · 2020Review
- O-1602, an Agonist of Atypical Cannabinoid Receptors GPR55, Reverses the Symptoms of Depression and Detrusor Overactivity in Rats Subjected to Corticosterone Treatment.Frontiers in pharmacology · 2020Article
- Brain activity of anandamide: a rewarding bliss?Acta pharmacologica Sinica · 2019Review
- Atypical cannabinoid ligands O-1602 and O-1918 administered chronically in diet-induced obesity.Endocrine connections · 2019Article
44 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeAtypical cannabinoids are thought to cause vasodilatation through an as-yet unidentified 'CBx' receptor. Recent reports suggest GPR55 is an atypical cannabinoid receptor, making it a candidate for the vasodilator 'CBx' receptor. The purpose of the present study was to test the hypothesis that human recombinant GPR55 is activated by atypical cannabinoids and mediates vasodilator responses to these agents. EXPERIMENTAL APPROACH: Human recombinant GPR55 was expressed in HEK293T cells and specific GTPgammaS activity was monitored as an index of receptor activation. In GPR55-deficient and wild-type littermate control mice, in vivo blood pressure measurement and isolated resistance artery myography were used to determine GPR55 dependence of atypical cannabinoid-induced haemodynamic and vasodilator responses. KEY
resultsAtypical cannabinoids O-1602 and abnormal cannabidiol both stimulated GPR55-dependent GTPgammaS activity (EC50 approximately 2 nM), whereas the CB1 and CB2-selective agonist WIN 55,212-2 showed no effect in GPR55-expressing HEK293T cell membranes. Baseline mean arterial pressure and heart rate were not different between WT and GPR55 KO mice. The blood pressure-lowering response to abnormal cannabidiol was not different between WT and KO mice (WT 20+/-2%, KO 26+/-5% change from baseline), nor was the vasodilator response to abnormal cannabidiol in isolated mesenteric arteries (IC50 approximately 3 micro M for WT and KO). The abnormal cannabidiol vasodilator response was antagonized equivalently by O-1918 in both strains.
conclusionsThese results demonstrate that while GPR55 is activated by atypical cannabinoids, it does not appear to mediate the vasodilator effects of these agents.
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Registered trials
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.