Abstract
Amyl nitrite was introduced in 1867 as the first molecule of a new class of agents for the treatment of angina pectoris. In the following 150 years, the nitric oxide pathway has been the subject of a number of pharmacological approaches, particularly since when this elusive mediator was identified as one of the most important modulators of vascular homeostasis beyond vasomotion, including platelet function, inflammation, and atherogenesis. While having potent antianginal and antiischemic properties, however, nitric oxide donors are also not devoid of side effects, including the induction of tolerance, and, as shown in the last decade, of oxidative stress and endothelial dysfunction. In turn, endothelial dysfunction is itself felt to be involved in all stages of atherogenesis, from the development of fatty streaks to plaque rupture and thrombosis. In the present review, we summarize the agents that act on the nitric oxide pathway, with a particular focus on their potentially beneficial antiatherosclerotic and unwanted pro-atherosclerotic effects.
Highlights
Atherosclerosis and its systemic correlates in the coronary, cerebral, and peripheral circulations represents the leading cause of death and disability worldwide [1]
The present review focuses on the effects of exogenous nitric oxide (NO) on atherogenesis, and the potential and limitations of NO-donor supplementation in the prevention of plaque growth and instabilization
An inappropriately high production of ROS from mitochondria can occur under pathological conditions, a phenomenon from mitochondria can occur under pathological conditions, a phenomenon during which electrons are deviated from the respiratory chain to molecular oxygen, triggering cross-activation of reactive oxygen species production from other cellular sources [5]
Summary
Atherosclerosis and its systemic correlates in the coronary, cerebral, and peripheral circulations represents the leading cause of death and disability worldwide [1]. The hypothesis that free radicals might have a role in this complex framework was raised as early as 1950 when oxidatively modified lipids and proteins were observed in vascular lesions This evidence led to the hypothesis that oxidative stress might be involved in the processes leading to atherogenesis and plaque instabilization (reviewed in [3]). At the end of the XXth century, studies demonstrated that another free radical, nitric oxide (NO), is among the most important mediators of vascular homeostasis, and that this elusive molecule with a very short half-life controls numerous vascular functions, including inhibition of smooth muscle proliferation, vascular inflammation, platelet activation, and vascular tone Based on this evidence, some authors brought forward the idea that exogenous sources of NO might recapitulate the antiatherosclerotic effects of endogenous NO, a hypothesis that has been supported in some, but not all the literature.
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