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INVITED REVIEW

Nitric oxide deficiency in chronic kidney disease

Department of Physiology and Functional Genomics, University of Florida, Gainesville, Florida

Submitted 10 September 2007 ; accepted in final form 4 October 2007

The overall production of nitric oxide (NO) is decreased in chronic kidney disease (CKD) which contributes to cardiovascular events and further progression of kidney damage. There are many likely causes of NO deficiency in CKD and the areas surveyed in this review are: 1. Limitations on substrate (L-Arginine) availability, probably due to impaired renal L-Arginine biosynthesis, decreased transport of L-Arginine into endothelial cells and possible competition between NOS and competing metabolic pathways, such as arginase. 2. Increased circulating levels of endogenous NO synthase (NOS) inhibitors, in particular asymmetric dimethylarginine (ADMA). Increased methylation of proteins and their subsequent breakdown to release free ADMA may contribute but the major culprit is probably reduced ADMA catabolism by the enzymes dimethylarginine dimethylaminohydrolases. 3. Reduced renal cortex abundance of the neuronal NOS (nNOS) protein correlates with injury while increasing nNOSβ abundance may provide a compensatory, protective response. Interventions that can restore NO production by targeting these various pathways are likely to reduce the cardiovascular complications of CKD as well as slowing the rate of progression.

arginase; asymmetric dimethylarginine; dimethylarginine dimethylaminohydrolase; L-arginine transporters; neuronal nitric oxide synthase

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