23
Views
5
CrossRef citations to date
0
Altmetric
Review

Nitric oxide therapy For cardiovascular disease

Pages 999-1005 | Published online: 25 Feb 2005
 

Abstract

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.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.