Anandamide and endothelium-derived hyperpolarizing factor act via a common vasorelaxant mechanism in rat mesentery.

We have recently proposed that an endocannabinoid, of which anandamide is prototypic, may be an endothelium-derived hyperpolarizing factor (EDHF). In the present study, both anandamide-induced and EDHF-mediated relaxations were insensitive to either charybdotoxin (100 nM) or apamin (500 nM) alone, but were inhibited by these agents in combination. These results point to EDHF and anandamide acting at a common site to cause vasorelaxation via K+ channel activation, and support our proposal that an endocannabinoid is an EDHF.