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Impact of the L-arginine-Nitric Oxide Pathway and Oxidative Stress on the Pathogenesis of the Metabolic Syndrome.

C R A, T M C B, C M, A C R, A C MR - Open Biochem J (2008)

Bottom Line: It occurs in genetically susceptible individuals with environmental influences and has serious economic and social consequences.Pharmacological and non-pharmacological therapies should be individualized and targeted to normalize its alterations of blood pressure, HDL cholesterol, triglycerides and glucose values.Emerging evidence is available that NO, inflammation and oxidative stress play important roles in the physiopathology of this syndrome.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Farmacologia e Psicobiologia, Instituto de Biologia, Av. 28 de Setembro 87 CEP 20551-030, Rio de Janeiro, Brazil.

ABSTRACT
The discovery of the physiological roles of nitric oxide has revolutionized the understanding of regulation of vascular tone, platelet adhesion and aggregation, and immune activation. Perhaps the most intriguing aspect of nitric oxide (NO) is that it is a gas that, in the absence of receptors, can regulate both normal physiological events and mediate cytotoxicity under pathological conditions. NO is produced from L-arginine by NO synthases (NOS), yielding L-citrulline and NO. The regulation of L-arginine pathway activity occurs at the level of NO production. The metabolic syndrome is a cluster of insulin resistance, elevated blood pressure, and atherogenic dyslipidemia, a common basis of cardiovascular disease. It occurs in genetically susceptible individuals with environmental influences and has serious economic and social consequences. Pharmacological and non-pharmacological therapies should be individualized and targeted to normalize its alterations of blood pressure, HDL cholesterol, triglycerides and glucose values. Despite the increasing prevalence of the metabolic syndrome in the last decades, there has been little progress in the understanding of the precise mechanisms involved in the pathogenesis of this syndrome and its complications. Emerging evidence is available that NO, inflammation and oxidative stress play important roles in the physiopathology of this syndrome. This review summarizes and evaluates the participation of the L-arginine-NO pathway and oxidative stress in the physiopathology of the metabolic syndrome and cardiovascular events at the systemic level, as well as the effects of exercise on this syndrome.

No MeSH data available.


Related in: MedlinePlus

NO=nitric oxide; NOS=nitric oxide synthase; GC=guanylase cyclase; GTP=guanosine triphosphate; cGMP=cyclic guanosine monophos-phate; ADMA=asymmetric dimethylarginine; L-NMMA.
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Figure 1: NO=nitric oxide; NOS=nitric oxide synthase; GC=guanylase cyclase; GTP=guanosine triphosphate; cGMP=cyclic guanosine monophos-phate; ADMA=asymmetric dimethylarginine; L-NMMA.

Mentions: NO is generated, in mammalian cells, from the amino acid L-arginine using the enzyme nitric oxide synthase (NOS), with the same spectral characteristic as the cytochrome P-450 family and an ED50 for L-arginine of about 6 µM [3, 8-10]. NO synthases include four prosthetic sets in their structure: flavin-adenine dinucleotide (FAD); flavin mononucleotide (FMN); tetrahydrobiopterin (H4 biopterin) and a haeme complex. The production of nitric oxide from L-arginine involves two monooxygenation steps requiring O2 and NADPH: an initial hydroxylation of L-arginine to generate N-hydroxyarginine and an oxidation leading to the formation of NO and citrulline [3, 8-10] (Fig. 1).


Impact of the L-arginine-Nitric Oxide Pathway and Oxidative Stress on the Pathogenesis of the Metabolic Syndrome.

C R A, T M C B, C M, A C R, A C MR - Open Biochem J (2008)

NO=nitric oxide; NOS=nitric oxide synthase; GC=guanylase cyclase; GTP=guanosine triphosphate; cGMP=cyclic guanosine monophos-phate; ADMA=asymmetric dimethylarginine; L-NMMA.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2570556&req=5

Figure 1: NO=nitric oxide; NOS=nitric oxide synthase; GC=guanylase cyclase; GTP=guanosine triphosphate; cGMP=cyclic guanosine monophos-phate; ADMA=asymmetric dimethylarginine; L-NMMA.
Mentions: NO is generated, in mammalian cells, from the amino acid L-arginine using the enzyme nitric oxide synthase (NOS), with the same spectral characteristic as the cytochrome P-450 family and an ED50 for L-arginine of about 6 µM [3, 8-10]. NO synthases include four prosthetic sets in their structure: flavin-adenine dinucleotide (FAD); flavin mononucleotide (FMN); tetrahydrobiopterin (H4 biopterin) and a haeme complex. The production of nitric oxide from L-arginine involves two monooxygenation steps requiring O2 and NADPH: an initial hydroxylation of L-arginine to generate N-hydroxyarginine and an oxidation leading to the formation of NO and citrulline [3, 8-10] (Fig. 1).

Bottom Line: It occurs in genetically susceptible individuals with environmental influences and has serious economic and social consequences.Pharmacological and non-pharmacological therapies should be individualized and targeted to normalize its alterations of blood pressure, HDL cholesterol, triglycerides and glucose values.Emerging evidence is available that NO, inflammation and oxidative stress play important roles in the physiopathology of this syndrome.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Farmacologia e Psicobiologia, Instituto de Biologia, Av. 28 de Setembro 87 CEP 20551-030, Rio de Janeiro, Brazil.

ABSTRACT
The discovery of the physiological roles of nitric oxide has revolutionized the understanding of regulation of vascular tone, platelet adhesion and aggregation, and immune activation. Perhaps the most intriguing aspect of nitric oxide (NO) is that it is a gas that, in the absence of receptors, can regulate both normal physiological events and mediate cytotoxicity under pathological conditions. NO is produced from L-arginine by NO synthases (NOS), yielding L-citrulline and NO. The regulation of L-arginine pathway activity occurs at the level of NO production. The metabolic syndrome is a cluster of insulin resistance, elevated blood pressure, and atherogenic dyslipidemia, a common basis of cardiovascular disease. It occurs in genetically susceptible individuals with environmental influences and has serious economic and social consequences. Pharmacological and non-pharmacological therapies should be individualized and targeted to normalize its alterations of blood pressure, HDL cholesterol, triglycerides and glucose values. Despite the increasing prevalence of the metabolic syndrome in the last decades, there has been little progress in the understanding of the precise mechanisms involved in the pathogenesis of this syndrome and its complications. Emerging evidence is available that NO, inflammation and oxidative stress play important roles in the physiopathology of this syndrome. This review summarizes and evaluates the participation of the L-arginine-NO pathway and oxidative stress in the physiopathology of the metabolic syndrome and cardiovascular events at the systemic level, as well as the effects of exercise on this syndrome.

No MeSH data available.


Related in: MedlinePlus