Nitroso–Redox Interactions in the Cardiovascular System

Up-regulation of A2B adenosine receptor in A2A adenosine receptor knockout mouse coronary artery

“…The authors suggested that it may be that L-NMAE is transported into the cell using either diffusion or a transport system other than cationic amino acid transporter used by L-NMA [28,29]. In addition, NO is a part of the complex redox system that are known to be heavily involved in multiple cardiovascular signal transduction systems, which regulate contractility, blood flow, and heart rate [30][31][32]. Nevertheless, both inhibitors demonstrated similar results in this study and their effect on heart rate is minimal.…”

Sepsis-induced cardiomyopathy: a review of pathophysiologic mechanisms

“…NO signaling by nitrosylation is fast, reversible, and affected by the overall nitroso-redox balance of the system [20]. The oxidase enzymes NADPH oxidase and xanthine oxidase, as well as mitochondrial oxidative phosphorylation, generate the biologically relevant reactive oxygen species superoxide, hydrogen peroxide and the hydroxyl radical [21]. Reactive oxygen species (ROS) can be cytotoxic at high levels through a number of mechanisms.…”

“…Progressive oxidation of these substrates is irreversible, rendering them incapable of interacting with NO, thereby disrupting physiologic NO signaling [21]. Furthermore, NOS isoforms may directly interact with ROS-generating enzymes in a regulatory manner, such that NOS deficiency results in uncontrolled ROS production [19,21]. Several animal models of heart failure have investigated the contributions of oxidative imbalance.…”

“…Two other studies illustrated how inhibition of xanthine oxidase (XO) with allopurinol improves parameters of endothelial function in smokers and diabetics, two populations prone to atherosclerosis and resultant endothelial dysfunction [23,24]. However, no trials in humans with CHF to date have shown that XO inhibition leads to significant improvements in symptoms, functional performance, or clinical outcomes [21].…”

Mortality in rheumatoid arthritis patients with heart failure: Comment on the article by Davis et al

“…In particular, reactive oxygen species such as superoxide anion, hydrogen peroxide, and the hydroxyl radical can provoke myocyte apoptosis and necrosis. Furthermore, these reactive species can induce endothelial dysfunction and arrhythmias through inactivation of nitric oxide and reduction of nitric oxide synthase activity (4,5). Davis et al recognize that RA patients have high levels of systemic inflammation (1), which could sustain the myocardiac "pro-arrhythmogenic" milieu, so that a higher rate of atrial fibrillation and fatal arrhythmia would be present in heart failure in RA patients.…”