Nitric oxide in the kidney: Physiological roles and regulation

Abstract

Physiological roles of nitric oxide (NO) in the kidney include the regulation of renal and glomerular haemodynamics, mediation of pressure natriuresis, maintenance of medullary perfusion, blunting of tubuloglomerular feedback (TGF), inhibition of tubular sodium reabsorption and modulation of renal sympathetic nerve activity. The net effect of NO in the kidney is to promote natriuresis and diuresis and NO plays an important role in the renal adaptation to variations of dietary salt intake. Reduction of NO production in the renal medulla, either pharmacologically or genetically, has a great impact on the delivery of blood to the medulla and on the long-term regulation of sodium excretion and blood pressure. Conversely, infusion of L-arginine to increase nitric oxide, abrogates hypertension and enhances medullary blood flow. It is evident that medullary NO production serves as an important counterregulatory factor to buffer vasoconstrictor hormone-induced reduction of medullary blood flow and tissue oxygen levels. Nitric oxide levels can also be controlled through its consumption by reactive oxygen species. This review will focus on NOS isoforms distribution and regulation and on NO roles in renal physiology. In addition, recent advances in the involvement of NOS isoforms on apoptosis induction and tubulo-interstitial fibrosis will be discussed.