Nitric Oxide and its Role in Cardiovascular Diseases

Abstract

Nitric oxide synthases (NOS) are the enzymes responsible for nitric oxide (NO) generation. NO is a free radical which reacts with various molecules to cause multiple biological effects. It is clear that the generation and actions of NO under physiological and pathophysiological conditions are exquisitely regulated and extend to almost every cell type and function within the circulation. While the molecule mediates many physiological functions, an excessive presence of NO is toxic to cells. The enzyme NOS, constitutively or inductively, catalyses the production of NO in several biological systems. NO is derived not only from NOS isoforms but also from NOS-independent sources. In mammals, to date, three distinct NOS isoforms have been identified: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). The molecular structure, enzymology and pharmacology of these enzymes have been well defined, and reveal critical roles for the NOS system in a variety of important physiological processes. This review focuses on recent advances in the understanding of the interactions between NOS enzymes and pathophysiology of cardiovascular diseases (CVD) and the role of NO agonists as potential therapeutic agents in treatment of CVD.

Low SOD activity is associated with overproduction of peroxynitrite and nitric oxide in patients with acute coronary syndrome

“…An elevation of NO• levels as it is seen in the current work, had been reported in many other pathological cases, such as hypertension, hypercholesterolemia, atherosclerosis, stroke, rheumatoid arthritis and diabetes [18,25,45,46]. In chronic heart disease, the accumulation of NO• may reflect its impaired synthesis and/or action [47]. It may be the result of compensatory excessive synthesis due to its diminished bioavailability or increased oxidative degradation.…”

Asymmetric Dimethylarginine (ADMA) and Symmetric Dimethylarginine (SDMA) Concentrations in Patients with Obesity and the Risk of Obstructive Sleep Apnea (OSA)

“…Asymmetric dimethylarginine (ADMA), a strong inhibitor of nitric oxide synthase, and symmetric dimethylarginine (SDMA) are toxic amino acids that inhibit nitric oxide (NO) production. The loss of NO production and bioactivity can be associated with development of pathological conditions such as hypertension or obstructive sleep apnea (OSA) [14,15]. Both of these conditions are characterized by an increased expression of pro-inflammatory cytokines and the production of reactive oxygen species (ROS), which are also commonly seen in obesity [16].…”

Effects of exercise and L-arginine intake on inflammation in aorta of high-fat diet induced obese rats

“…Nitric oxide, a product of arginine, is generated by the three isomorphic forms of nitric oxide synthase (NOS): neuronal NOS (nNOS), inducible NOS (iNOS) and endothelial NOS (eNOS), which are widely expressed in virtually all vascular cell types 18 , 19 , 20 . NO influences a number of metabolic, biosynthetic, signaling, and membrane transport processes 19 , 21 , and one of itsimportant roles is regulating vascular tone and structure 19 , 22 . In previous reports, acute and chronic arginine treatment improve endothelial function in hypercholesterolemia and atherosclerosis models 23 .…”

“…Increased plasma arginine concentration leads to increased production of both vascular and systemic NO 24 , 25 , 26 . Stimulated NO production leads to relaxed vascular smooth muscle cells 19 , 27 ,and reduced bioavailability of NO as a result of either decreased NOS production or increased breakdown by reactive oxygen species (ROS) is implicated in the development of various vascular disorders 28 , 29 , 30 .…”