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Arginine and nitric oxide synthase: Regulatory mechanisms and cardiovascular aspects
Author(s) -
Lorin Julie,
Zeller Marianne,
Guilland JeanClaude,
Cottin Yves,
Vergely Catherine,
Rochette Luc
Publication year - 2014
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201300033
Subject(s) - tetrahydrobiopterin , nitric oxide , nitric oxide synthase , oxidative stress , arginine , pharmacology , superoxide , endothelial dysfunction , bioavailability , biochemistry , endocrinology , medicine , chemistry , amino acid , enzyme
l ‐ A rginine ( l ‐ A rg) is a conditionally essential amino acid in the human diet. The most common dietary sources of l ‐ A rg are meat, poultry and fish. l ‐ A rg is the precursor for the synthesis of nitric oxide ( NO ); a key signaling molecule via NO synthase ( NOS ). Endogenous NOS inhibitors such as asymmetric‐dimethyl‐ l ‐ A rg inhibit NO synthesis in vivo by competing with l ‐ A rg at the active site of NOS . In addition, NOS possesses the ability to be “uncoupled” to produce superoxide anion instead of NO . Reduced NO bioavailability may play an essential role in cardiovascular pathologies and metabolic diseases. l ‐ A rg deficiency syndromes in humans involve endothelial inflammation and immune dysfunctions. Exogenous administration of l ‐ A rg restores NO bioavailability, but it has not been possible to demonstrate, that l ‐ A rg supplementation improved endothelial function in cardiovascular disease such as heart failure or hypertension. l ‐ A rg supplementation may be a novel therapy for obesity and metabolic syndrome. The utility of l ‐ A rg supplementation in the treatment of l ‐ A rg deficiency syndromes remains to be established. Clinical trials need to continue to determine the optimal concentrations and combinations of l ‐ A rg, with other protective compounds such as tetrahydrobiopterin ( BH 4 ), and antioxidants to combat oxidative stress that drives down NO production in humans.