| Abstrakt: |
Endothelial dysfunction due to reduced availability of nitric oxide (NO) is an early step in the course of atherosclerotic vascular disease. NO is synthesized from the amino acid L-arginine by the action of the NO synthase (NOS), which can be blocked by endogenous inhibitors such as asymmetric dimethylarginine (ADMA). In laboratory animals, administration of ADMA significantly reduces NO generation, and causes an increase of blood pressure and renal vascular resistance. In clinical studies, a strong correlation between increased ADMA blood levels and impaired endothelial-dependent vasodilatation, and cardiovascular morbidity and mortality has been documented in different populations, including in patients with renal disease. Thus, ADMA seems to be the culprit, and not just an innocent biochemical bystander, of the atherosclerotic disease process. Moreover, reduced NO availability is involved in the progression of renal disease, and increased ADMA blood levels may contribute to this process. Interventions that lower ADMA blood levels in renal patients could, therefore, modulate their atherogenic profile and interfere with progression of renal failure. |
