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Background--Nitric oxide (NO) is a potent chemical mediator involved in many functions. In vivo production of NO is thought to be regulated by endogenous analogues of L-arginine: asymmetric dimethylarginine (ADMA).
Aim--To examine the effect of renal function and dialysis on the serum concentrations of ADMA and symmetric dimethylarginine (SDMA).
Methods--Blood samples were obtained from nine healthy subjects, patients with renal failure before (n = 17) and after haemodialysis (n = 9), nine patients on chronic ambulatory peritoneal dialysis (CAPD), and 13 patients with chronic renal failure on conservative treatment. Serum samples were extracted using a solid phase cation exchange column and the extracts were analysed by high performance liquid chromatography (HPLC).
Results--Serum concentrations of ADMA in patients with renal failure (mean, 1.04 [micro]mol/litre; SD, 0.17) were significantly higher than those of controls (mean, 0.61 [micro]mol/litre; SD, 0.13). Haemodialysis significandy decreased the serum concentration by 36% (before dialysis: mean 0.99 (SD, 0.25) [micro]mol/litre). after dialysis: mean, 0.63 (SD, 0.15) [micro] Serum SDMA concentrations were higher in patients with renal failure, and haemodialysis decreased the concentration by 60%. There was no difference in serum arginine concentrations between the groups.
Conclusion--Serum concentrations of ADMA are increased in renal failure and haemodialysis reduces the concentration.
Keywords: chronic renal failure; dialysis; nitric oxide; arginine; dimethylarginines
Nitric oxide (NO), a potent chemical mediator synthesised from L-arginine by a family of NO synthases, is involved in many functions including regulation of vascular tone, neurotransmission, and host defence.  In the blood vessels, basal release of NO is important in the maintenance of vascular tone and blood pressure.  Abnormalities in NO production have been implicated in many diseases including hypertension, [3 4] pre-eclampsia, [5, 6] multiple sclerosis,  hypercholesterolaemia,  septic shock,  and renal failure.  NO is synthesised by the conversion of L-arginine to L-citrulline by the enzyme NO synthase. One of the factors determining the activity of the enzyme is the availability of the substrate L-arginine, which is transported into the cell by an amino acid transporter. The transport of L-arginine can be blocked experimentally by its analogue [N.sup.G]-methyl-L-arginine (L-NMMA). 
It has been suggested that endogenous analogues of L-arginine might be involved in the regulation of the in vivo production of NO. One of these, [N.sup.G],[N.sup.G]-dimethyl-L-arginine (asymmetric dimethylarginine; ADMA), has been shown to be present in human urine, plasma,  and tissues,  and to be synthesised by endothelial cells.  ADMA has been shown to inhibit NO synthesis in vitro  and has been suggested to play a role in regulating …