Vascular effects of delta 9-tetrahydrocannabinol (THC), anandamide and N-arachidonoyldopamine (NADA) in the rat isolated aorta.

  title={Vascular effects of delta 9-tetrahydrocannabinol (THC), anandamide and N-arachidonoyldopamine (NADA) in the rat isolated aorta.},
  author={Saoirse Elizabeth O'Sullivan and David A. Kendall and Michael D Randall},
  journal={European journal of pharmacology},
  volume={507 1-3},

Time-Dependent Vascular Effects of Endocannabinoids Mediated by Peroxisome Proliferator-Activated Receptor Gamma (PPARγ)

Data indicate that endocannabinoids cause time-dependent, PPARγ-mediated vasorelaxation, which may represent a novel mechanism by which endoc cannabinoidoids are involved in vascular regulation.

Δ9-tetrahydrocannabinol treatment improved endothelium-dependent relaxation on streptozotocin/nicotinamide-induced diabetic rat aorta.

Results suggested that THC improved endothelium-dependent relaxation in STZ/NIC induced diabetic rat aorta and that these effects were mediated at least in part, by control of hyperglycemia and enhanced endothelial nitric oxide bioavailability.

Effects of hypertension on vasorelaxation to endocannabinoids in vitro.




Anandamide-induced vasorelaxation in rabbit aortic rings has two components: G protein dependent and independent.

In the rabbit aorta, methanandamide-induced vasorelaxation exhibits two components: in endothelium-intact rings, an SR141716A-sensitive, non-CB(1) receptor component that requires pertussis toxin-sensitive G proteins and nitric oxide (NO) production; and in endot Helium-denuded rings, a component that is mediated by VR(1).

Anandamide and delta 9-THC dilation of cerebral arterioles is blocked by indomethacin.

Results show that AN and delta 9-THC can modulate cerebral arterioles, likely by stimulating release and metabolism of endogenous arachidonic acid, and whether dilation is due to vasodilator eicosanoids, or other vasoactive agents whose synthesis or release is cyclooxygenase dependent, is uncertain.

Characterisation of the vasorelaxant properties of the novel endocannabinoid N‐arachidonoyl‐dopamine (NADA)

The results of the present study demonstrate for the first time that NADA is a potent vasorelaxant.

Selective ligands and cellular effectors of a G protein-coupled endothelial cannabinoid receptor.

Findings indicate that abn-cbd is a selective agonist and that O-1918 is a Selective, silent antagonist of an endothelial "anandamide receptor", which is distinct from CB(1) or CB(2) receptors and is coupled through G(i)/G(o) to the PI3 kinase/Akt signaling pathway.

Endothelium-independent relaxation to cannabinoids in rat-isolated mesenteric artery and role of Ca2+ influx.

The aminoalkylindoles relax rat small mesenteric artery mainly by inhibiting Ca(2+) influx into vascular smooth muscle and inhibited CaCl(2) contractions in methoxamine-stimulated vessels previously depleted of intracellular Ca( 2+).

Mechanisms of vasorelaxation to testosterone in the rat aorta.

Inhibition of the production of endothelium‐derived hyperpolarizing factor by cannabinoid receptor agonists

Results suggest that the activation of endothelial CB1 receptors appears to be negatively coupled to the production of EDHF, and the effects of cannabinoid CB1 receptor agonists are investigated.

Vanilloid receptors on sensory nerves mediate the vasodilator action of anandamide

It is shown that the vasodilator response to anandamide in isolated arteries is capsaicin-sensitive and accompanied by release of calcitonin-gene-related peptide (CGRP), which indicates that the vanilloid receptor may be another molecular target for endogenousAnandamide, besides cannabinoid receptors, in the nervous and cardiovascular systems.