Accumulation of an endogenous inhibitor of nitric oxide synthesis in chronic renal failure.

摘要: Nitric oxide (NO), synthesised from L-arginine, contributes to the regulation of blood pressure and host defence. We describe in-vitro in-vivo evidence that NO synthesis can be inhibited by an endogenous compound, NG,NG-dimethylarginine (asymmetrical dimethylarginine, ADMA). In man, this inhibitor is found in plasma more than 10 mg excreted urine over 24 h. However, patients with end-stage chronic renal failure, who have little or no output, elimination blocked circulating concentrations rise sufficiently inhibit synthesis. Accumulation ADMA, leading impaired synthesis, might contribute hypertension immune dysfunction associated failure.