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 limited NO bioavailability may contribute to a raft of vascular pathologies while a failure of peripheral 'nitrergic' neurovasodilator tone is implicated in erectile dysfunction. In addition to the established NO therapy exemplified by the use of nitrovasodilators, the endogenous NO pathway can now be therapeutically modulated to optimise endothelial or peripheral neuronal vasodilator function by inhibiting PDEV. A similar modulation of the NO pathway 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.