title: Endocannabinoids as mediators in the heart: a potential target for therapy of remodelling after myocardial infarction?
abstract: Endocannabinoid production by platelets and macrophages is increased in circulatory shock. This may be protective of the cardiovascular system as blockade of CB(1) cannabinoid receptors exacerbates endothelial dysfunction in haemorrhagic and endotoxin shock and reduces survival. Now evidence suggests that blockade of CB(1) receptors starting 24 h after myocardial infarction in rats has a deleterious effect on cardiac performance, while use of a nonselective cannabinoid receptor agonist prevents hypotension and reduces endothelial dysfunction, although left ventricular end diastolic pressure is elevated. Cannabinoids and endocannabinoid systems may therefore present useful targets for therapy following myocardial infarction.
authors.affiliation: Department of Pharmacology, University of Cambridge, Tennis Court Road, Cambridge CB2 1PD. crh1@cam.ac.uk
authors.forename: C Robin
authors.initials: CR
authors.lastname: Hiley
authors.forename: William R
authors.initials: WR
authors.lastname: Ford
mesh_terms: D063385:Cannabinoid Receptor Modulators / Q000627:therapeutic use*; D063388:Endocannabinoids; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology*; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy*; D043882:Receptors, Cannabinoid / Q000187:drug effects*; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: D063385:Cannabinoid Receptor Modulators; D063388:Endocannabinoids; D043882:Receptors, Cannabinoid