The Nitric Oxide Pathway and Oxidative Stress in Heart Failure

Abstract

). The neurohormonal changes that accompany and exacerbate CHF have been the subject of much recent study, and, as a result, we have a greater understanding of heart failure and potential targets for therapeutic intervention. Angiotensin-converting enzyme (ACE) inhibition and β-adrenergic receptor blockade are examples of therapeutic interventions that target specific neurohormonal abnormalities and have significant impact on morbidity and mortality in heart failure patients. As we comprehend more about the hormonal pathophysiology of heart failure, we will progress in our ability to treat and/or prevent this disease. This review will focus on the current perception of the NO . pathway in heart failure. It will discuss regulation of the enzyme that synthesizes NO . , nitric oxide synthase (NOS), as well as modulation of NO . bioavailability. Finally, the review will address the effect of oxidative stress on the NO . pathway.Oxidative Stress and the NO . PathwayOxidative stress is a term used to describe a condition in which cells are exposed to excessive levels of either molecular oxygen or chemical derivatives of oxygen

Cardiac enkephalins attenuate vagal bradycardia: interactions with NOS-1-cGMP systems in canine sinoatrial node

“…In support of this concept, exercise training-mediated improvements in vagal control of heart rate were well correlated with increased atrial NOS activity (17). Furthermore, pathological states such as hypertension and congestive heart failure are both associated with impaired NO production (16,26) and impaired vagal control of the heart.…”

“…The pericardium was opened and the upper pericardial margins were sutured to the body wall to support and stabilize the heart. Because NO reportedly also reduces norepinephrine release from cardiac sympathetic nerves, the primary cardiac sympathetic nerves were severed bilaterally (26). The sympathetic nerves were isolated as they exit the stellate ganglia (ansa subclavia).…”

Modulation of inflammation and angiogenesis and changes in ECM GAG-activity via dual delivery of nucleic acids

“…Endothelial nitric oxide synthase (eNOS) is a pro-angiogenic enzyme that acts as a catalyst in the reaction of Larginine to L-citruline, resulting in the formation of nitric oxide (NO) [23]. NO promotes relaxation of blood vessels and the mobilization of endothelial progenitor cells (EPCs), an important step in the formation of new blood vessels [24,25]. In addition, NO has been shown to reduce IL-6 expression at high doses, in an NF-kB dependent pathway [26].…”

Oxidative stress and heart disease: Cardiac dysfunction, nutrition, and gene therapy

“…O 2 •-is a powerful oxidant formed by the reduction of molecular oxygen during cellular metabolism and by enzymes such as NADPH oxidase and xanthine oxidase [2][3][4]. The production of this free radical leads to the subsequent formation of other radicals.…”

“…More specifically, O 2 •-reacts with H 2 O 2 to form • OH and also reacts readily with NO • to produce ONOO -, a powerful oxidant [5,6]. H 2 O 2 is produced via the enzymatic or spontaneous dismutation of O 2 •- [3,7], while NO • is formed through the L-arginine pathway and is catalyzed by nitric oxide synthase (NOS) [3]. These free radicals tend to initiate chain reactions resulting in irreversible changes in lipids or proteins, leading to potential cellular dysfunction and toxicity [8].…”