Why the study?
Endothelial dysfunction with reduced nitric oxide generation is implicated in atherosclerosis, motivating exploration of NO donor drugs for prevention and treatment.
Do drugs that donate NO or increase endogenous NO availability provide therapeutic benefit in the prevention and treatment of atherosclerosis?
Do drugs that donate NO or increase endogenous NO availability provide therapeutic benefit in the prevention and treatment of atherosclerosis?
Nitric oxide donors and drugs that increase endogenous NO availability may offer therapeutic benefits in preventing and treating atherosclerosis.
NO donors and enhancers merit prospective trials in atherosclerosis; leaves open clinical adoption pending randomized data.
Well-known risk factors for atherosclerosis include hypercholesterolaemia, hypertension, diabetes, and smoking. These conditions are associated with endothelial dysfunction, which itself is associated with reduced endothelial generation of nitric oxide (NO). This is an overview of the implications of NO generation in atherosclerosis and of the potential therapeutic benefit of drugs which donate NO, such as organic nitrates, nicorandil, and sydnonimines, or those which increase the availability of endogenous NO, such as statins, angiotensin-converting enzyme inhibitors, L-arginine, and tetrahydrobiopterin.
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Herman et al. (2005) studied this question.
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