Asymmetric dimethylarginine, endothelial dysfunction and renal disease.

摘要: l-Arginine (Arg) is oxidized to l-citrulline and nitric oxide (NO) by the action of endothelial synthase (NOS). In contrast, protein-incorporated Arg residues can be methylated with subsequent proteolysis giving rise methylarginine compounds, such as asymmetric dimethylarginine (ADMA) that competes for binding NOS. Most ADMA degraded dimethyaminohydrolase (DDAH), distributed widely throughout body regulates levels and, therefore, NO synthesis. recent years, several studies have suggested increased are a marker atherosclerotic change, used assess cardiovascular risk, consistent being predominantly absorbed cells. an important messenger molecule involved in numerous biological processes, its activity essential understand both pathogenic therapeutic mechanisms kidney disease renal transplantation. production reduced patients because their elevated associated DDAH activity. These factors contribute dysfunction, oxidative stress progression damage, but there treatments may effectively reduce disease. Available data on controls patients, adults children, also summarized this review.