Effect of chronic renal failure on nitric oxide metabolism

Abstract

Chronic renal failure (CRF) is associated with hypertension, endothelial dysfunction, and a strong propensity for arteriosclerotic cardiovascular disease. Nitric oxide (NO) is an endogenous modulator with diverse biological functions. Chronic inhibition of NO synthases (NOS) has been shown to cause hypertension and vasculopathy. In light of these considerations, numerous studies have explored the effect of CRF on NO metabolism with the assumption that NO deficiency may be involved in the pathogenesis of cardiovascular and other consequences of uremia. The purpose of this review is to provide a brief overview of the effect of CRF on (1) the bioavailability of NO substrate, L-arginine; (2) the expression of NOS isoforms in the relevant organs; (3) the interaction of NO with reactive oxygen species that are known to be increased in CRF, and (4) the accumulation of uremic inhibitors of NOS.