Nitric oxide therapy for cardiovascular disease

Endothelium-derived NO is acknowledged as a key mediator of cardiovascular homeostasis. Indeed, an impairment in endothelial function resulting in lim ited NO bioavailability may contribute to a raft of vascular pathologies wh ile a failure of peripheral 'nitrergic' neurovasodilator tone is implicated in erectile dysfunction. In addition to the established NO therapy exempli fied by the use of nitrovasodilators, the endogenous NO pathway can now be therapeutically modulated to optimise endothelial or peripheral neuronal va sodilator function by inhibiting PDEV. A similar modulation of the NO pathw ay may also be clinically viable through the supplementation of precursors and cofactors of NO synthesis, the upregulation of endothelial NO synthase (eNOS) and the transfection of NOS genes to the vasculature.