ArticleBritish journal of pharmacology2004
Characterisation of the vasorelaxant properties of the novel endocannabinoid N-arachidonoyl-dopamine (NADA).
Article in British journal of pharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 65 citations in OpenAlex.
- N-Oleoyl dopamine induces IL-10 via central nervous system TRPV1 and improves endotoxemia and sepsis outcomes.Journal of neuroinflammation · 2022Article
- Review
- Endo-cannabinoids system and the toxicity of cannabinoids with a biotechnological approach.EXCLI journal · 2017Review
- Identification of N-arachidonoyl dopamine as a highly biased ligand at cannabinoid CB1 receptors.British journal of pharmacology · 2016Article
- The endocannabinoid/endovanilloid N-arachidonoyl dopamine (NADA) and synthetic cannabinoid WIN55,212-2 abate the inflammatory activation of human endothelial cells.The Journal of biological chemistry · 2014Article
- Vascular targets for cannabinoids: animal and human studies.British journal of pharmacology · 2014Review
- Cyclooxygenase metabolism mediates vasorelaxation to 2-arachidonoylglycerol (2-AG) in human mesenteric arteries.Pharmacological research · 2014Article
- Is the cardiovascular system a therapeutic target for cannabidiol?British journal of clinical pharmacology · 2013Review
- N-acyl amino acids and N-acyl neurotransmitter conjugates: neuromodulators and probes for new drug targets.British journal of pharmacology · 2010Review
- N-arachidonoyl glycine, an endogenous lipid that acts as a vasorelaxant via nitric oxide and large conductance calcium-activated potassium channels.British journal of pharmacology · 2010Article
- Cannabinoids for clinicians: the rise and fall of the cannabinoid antagonists.European journal of endocrinology · 2009Review
- Modulation of cannabinoid receptor activation as a neuroprotective strategy for EAE and stroke.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2009Review
- Inhibition of human recombinant T-type calcium channels by the endocannabinoid N-arachidonoyl dopamine.British journal of pharmacology · 2009Article
- Article
- Vascular pharmacology of a novel cannabinoid-like compound, 3-(5-dimethylcarbamoyl-pent-1-enyl)-N-(2-hydroxy-1-methyl-ethyl)benzamide (VSN16) in the rat.British journal of pharmacology · 2007Article
- Oxidative metabolism of lipoamino acids and vanilloids by lipoxygenases and cyclooxygenases.Archives of biochemistry and biophysics · 2007Article
- Cannabinoids as therapeutic agents in cardiovascular disease: a tale of passions and illusions.British journal of pharmacology · 2007Article
- The endocannabinoid system as an emerging target of pharmacotherapy.Pharmacological reviews · 2006Review
- Vasorelaxant effects of oleamide in rat small mesenteric artery indicate action at a novel cannabinoid receptor.British journal of pharmacology · 2006Article
- N-arachidonoyl L-serine, an endocannabinoid-like brain constituent with vasodilatory properties.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. We have investigated the vascular effects of N-arachidonoyl-dopamine (NADA), a novel endocannabinoid/vanilloid. NADA caused vasorelaxant effects comparable to those of anandamide in small mesenteric vessels (G3), the superior mesenteric artery (G0) and in the aorta. 2. In G3, addition of N(G)-nitro-l-arginine methyl ester (300 microm) or the dopamine (D(1)) receptor antagonist (SCH23390, 1 microm) did not affect responses to NADA. In the presence of 60 mm KCl, after de-endothelialisation, or after K(+) channel inhibition with charybdotoxin (100 nm) and apamin (500 nm), relaxant responses to NADA were inhibited. 3. In G3, pretreatment with the vanilloid receptor (VR) agonist capsaicin (10 microm) or the VR antagonist capsazepine (10 microm) reduced vasorelaxation to NADA. 4. In G3, application of the CB(1) antagonist SR141716A at 1 microm but not 100 nm reduced the potency of NADA. Another CB(1) antagonist, AM251 (100 nm and 1 microm), did not affect vasorelaxation to NADA. After endothelial denudation, SR141716A (1 microm) did not reduce the responses further. A combination of capsaicin and SR141716A (1 microm) reduced vasorelaxation to NADA further than with capsaicin pretreatment alone. The novel endothelial cannabinoid (CB) receptor antagonist O-1918 opposed vasorelaxation to NADA in G3. 5. In the superior mesenteric artery (G0), vasorelaxation to NADA was not dependent on an intact endothelium and was not sensitive to O-1918, but was sensitive to capsaicin and SR141716A or AM251 (both 100 nm). 6. The results of the present study demonstrate for the first time that NADA is a potent vasorelaxant. In G3, the effects of NADA are mediated by stimulation of the VR and the novel endothelial CB receptor, while in G0, vasorelaxation is mediated through VR(1) and CB(1) receptors.
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