Michael D. Randall

TL;DR: It is reported that EDHF-mediated relaxations in the rat mesenteric arterial bed are blocked by a highly selective cannabinoid receptor antagonist, SR141716A, consistent with EDHF being a cannabinoid-like substance, and anandamide is a potent vasorelaxant in the mesentery, acting via a hyperpolarizing mechanism.

TL;DR: The endocannabinoid N‐arachidonoylethanolamide (anandamide) is co‐synthesized with other N‐acylethanolamides, namely N‐palmitoylethanlamide (PEA) and N‐oleoylethanolsamide (OEA), which have been shown to potentiate anandamide responses (so‐called ‘entourage effects’) in non‐vascular tissues.

TL;DR: The findings suggest that cannabinoids derived from arachidonic acid gain access to the endothelial cytosol via a transporter mechanism and subsequently stimulate relaxation by promoting diffusion of an to adjacent smooth muscle cells via gap junctions.

TL;DR: The cardiovascular actions of cannbinoids are complex and in conscious animals, the picture is one of bradycardia followed by pressor responses, but clearly the responses to cannabinoids are dependent on the experimental conditions and synthetic cannabinoids and endocannabinoids exhibit different pharmacologies.

TL;DR: Results show that cannabidiol binds to and activates PPARgamma, which partially underlies the time-dependent vascular effects of cannabdiol, however, cannABidiol-induced vasorelaxation in the rat isolated aorta appears to be largely due to calcium channel inhibition.