Relationship of asymmetric dimethylarginine to dialysis treatment and atherosclerotic disease

摘要: Relationship of asymmetric dimethylarginine to dialysis treatment and atherosclerotic disease. Asymmetric (ADMA) is an endogenous inhibitor endothelial nitric oxide (NO) synthase. Its concentration elevated in patients with end-stage renal disease (ESRD), part because it excreated via the kidneys. In addition, ADMA degraded by enzyme dimethylaminohydrolase (DDAH), which hydrolyzes L-citrulline dimethylamine. Activity DDAH decreased oxidized low density lipoprotein (LDL) or tumor necrosis factor-α (TNF-α) vitro yielding increased levels ADMA. Furthermore, plasma are hyperhomocyst(e) inemia hypertensive on a high salt diet. Data from several experimental studies suggest that concentrations pathophysiologically range (3 10 μmol/L) significantly inhibit vascular NO formation synthase presence L-arginine isolated human blood vessels, cultured macrophages, cells. It has been well demonstrated accumulates chronic failure. Although there controversy concerning absolute ADMA, all authors found two-to sixfold increase failure as compared controls. Different strategies differentially affect levels. The atherosclerosis associated higher normal function patients, but this phenomenon may be unrelated handling Reduced elaboration secondary accumulation important pathogenic factor for new uremic toxin. Clinical effect needed further elucidate its pathophysiological role uremia.