ArticleBritish journal of pharmacology2010
N-arachidonoyl glycine, an endogenous lipid that acts as a vasorelaxant via nitric oxide and large conductance calcium-activated potassium channels.
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 65 citations in OpenAlex.
- Big conductance calcium-activated potassium channel openers control spasticity without sedation.British journal of pharmacology · 2017Trial
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- CYP4F2 is a human-specific determinant of circulating N-acyl amino acid levels.The Journal of biological chemistry · 2023Article
- Pharmacognosy and Effects of Cannabinoids in the Vascular System.ACS pharmacology & translational science · 2022Review
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- GPR18-Mediated Relaxation of Human Isolated Pulmonary Arteries.International journal of molecular sciences · 2022Article
- Potassium channels as molecular targets of endocannabinoids.Channels (Austin, Tex.) · 2021Review
- Cannabinoids-A New Perspective in Adjuvant Therapy for Pulmonary Hypertension.International journal of molecular sciences · 2021Review
- The GPR18 Agonist PSB-KD-107 Exerts Endothelium-Dependent Vasorelaxant Effects.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Bioactive Lipids in MSCs Biology: State of the Art and Role in Inflammation.International journal of molecular sciences · 2021Review
- Article
- Protective Effect of N-Arachidonoyl Glycine-GPR18 Signaling after Excitotoxical Lesion in Murine Organotypic Hippocampal Slice Cultures.International journal of molecular sciences · 2019Article
- Anandamide and endocannabinoid system: an attractive therapeutic approach for cardiovascular disease.Therapeutic advances in cardiovascular disease · 2018Review
- The quest for endothelial atypical cannabinoid receptor: BKVascular pharmacology · 2018Article
- Abnormal cannabidiol confers cardioprotection in diabetic rats independent of glycemic control.European journal of pharmacology · 2018Article
- Direct activation of CaEuropean journal of pharmacology · 2017Article
- The Effect of Chronic Activation of the Novel Endocannabinoid Receptor GPR18 on Myocardial Function and Blood Pressure in Conscious Rats.Journal of cardiovascular pharmacology · 2017Article
- Pharmacological profiling of the hemodynamic effects of cannabinoid ligands: a combined in vitro and in vivo approach.Pharmacology research & perspectives · 2015Article
- Endothelial atypical cannabinoid receptor: do we have enough evidence?British journal of pharmacology · 2014Review
- The cannabinoid acids, analogs and endogenous counterparts.Bioorganic & medicinal chemistry · 2014Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeN-arachidonoyl glycine (NAGly) is an endogenous lipid that is structurally similar to the endocannabinoid, N-arachidonoyl ethanolamide (anandamide). While NAGly does not activate cannabinoid receptors, it exerts cannabimimetic effects in pain regulation. Here, we have determined if NAGly, like anandamide, modulates vascular tone. EXPERIMENTAL APPROACH: In rat isolated small mesenteric arteries, the relaxant responses to NAGly were characterized. Effects of N-arachidonoyl serine and N-arachidonoyl gamma-aminobutyric acid were also examined. KEY
resultsIn endothelium-intact arteries, NAGly-induced relaxation (pEC(50%)= 5.7 +/- 0.2; relaxation at 30 microM = 98 +/- 1%) was attenuated by l-NAME (a nitric oxide synthase inhibitor) or iberiotoxin [selective blocker of large conductance Ca(2+)-activated K(+) channels (BK(Ca))], and abolished by high extracellular K(+) concentration. Endothelial removal reduced the potency of NAGly, and the resultant relaxation was inhibited by iberiotoxin, but not l-NAME. NAGly responses were sensitive to the novel cannabinoid receptor antagonist O-1918 independently of endothelial integrity, whereas pertussis toxin, which uncouples G(i/o) proteins, attenuated NAGly relaxation only in endothelium-intact arteries. Treatments with antagonists for CB(1), CB(2) and TRPV1 receptors, or inhibitors of fatty acid amide hydrolase and COX had no effect. The two other arachidonoyl amino acids also induced iberiotoxin- and L-NAME-sensitive relaxations. CONCLUSION AND IMPLICATIONS: NAGly acts as a vasorelaxant predominantly via activation of BK(Ca) in rat small mesenteric arteries. We suggest that NAGly activates an unknown G(i/o)-coupled receptor, stimulating endothelial release of nitric oxide which in turn activates BK(Ca) in the smooth muscle. In addition, NAGly might also activate BK(Ca) through G(i/o)- and nitric oxide-independent mechanisms.
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