Nitric oxide mechanisms in the pathogenesis of global risk.
Identification and management of cardiovascular risk factors, such as hypertension, diabetes mellitus, and dyslipidemia, is essential not only for prevention of cardiovascular disease, but also for slowing the progression of existing cardiovascular disease. A major underlying mechanism that links various cardiovascular risk factors and manifestations of cardiovascular disease is endothelial dysfunction, characterized by impaired nitric oxide bioactivity. Oxidative stress is an important cause of impaired nitric oxide bioactivity, and a major pathogenic mechanism of atherosclerosis. Several pharmacologic therapies, including angiotensin-converting enzyme inhibitors, calcium channel blockers, statins, and the vasodilating beta blocker nebivolol, have been shown to enhance nitric oxide bioactivity and improve endothelial function. This effect may help explain the cardioprotective benefits of these agents and may stimulate further use of nitric oxide modulation for the treatment of cardiovascular risk factors and manifestations of cardiovascular disease.[1]References
- Nitric oxide mechanisms in the pathogenesis of global risk. Mason, R.P. Journal of clinical hypertension (Greenwich, Conn.) (2006) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Use
The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.








