¹Department of Pharmacology, University of Cambridge, Cambridge, UK

Correspondence: Dr CR Hiley, Department of Pharmacology, University of Cambridge, Tennis Court Road, Cambridge CB2 1PD, UK. E-mail: crh1@cam.ac.uk

Received 11 July 2007; Accepted 20 July 2007; Published online 20 August 2007.

Abstract

CB₁ and CB₂ receptors mediate most responses to cannabinoids but not some of the cardiovascular actions of endocannabinoids such as anandamide and virodhamine, or those of some synthetic agents, like abnormal cannabidiol (abn-cbd). These agents induce vasorelaxation which is antagonised by rimonabant but only at high concentrations relative to those required to block CB₁ receptors. Vasorelaxation to anandamide is sensitive to Pertussis toxin (though that to abn-cbd is not), and so is thought to be mediated by a G protein-coupled receptor through G_i/o. An orphan receptor, GPR55, apparently a cannabinoid receptor, is activated by abn-cbd, but is not the receptor mediating vasorelaxation to this agent, as the response persists in vessels from GPR55 knockout mice. However, the activity of anandamide in GPR55 knockout mice is not yet reported and so the role of GPR55 as a cannabinoid receptor mediating vascular responses has yet to be finalised.