Nitric oxide in the developing kidney

Abstract

Although nitric oxide (NO) has a well-established role in regulating renal function in the adult, recent studies point to perhaps an even more critical role for NO in maintaining basal renal blood flow (RBF) and glomerular filtration rate (GFR) in the developing kidney. The immature kidney has enhanced renal hemodynamic and functional responses to stimulation and inhibition of NO synthesis when compared with the adult, and these increased responses are not mediated by prostaglandins. Increased intrarenal activity of NO in the developing kidney counter-regulates the highly activated renin angiotensin system by modulating the angiotensin II-mediated vasoconstriction of the developing renal vasculature, the angiotensin II effects on GFR, as well as renin release. Localization studies demonstrate that NO acts on neonatal RBF and stabilization of GFR through an intrarenal distribution of the synthesizing enzyme, nitric oxide synthase, that is different from that of the adult. The developing kidney is dependent on NO to maintain RBF and GFR during periods of hypoxemia, protecting against renal injury, such as acute renal failure. In summary, NO is vital in the developing kidney to maintain normal physiological function and to protect the immature kidney during pathophysiological stress.

Glomerular and tubular responses toNG-nitro-l-arginine methyl ester are age dependent in conscious lambs

“…These findings provided evidence that the role of NO in modulating renal vascular tone under physiological conditions predominates early in life. This age-dependent effect of L-NAME on RVR was confirmed in the present study and confirms previous observations in anesthetized newborn animals (34). In addition, we previously demonstrated age-dependent effects on renal vascular tone of intra-arterial administration of ACh (29), a muscarinic agonist known to elicit a vasodilation by producing NO.…”

Interaction of Endothelial Nitric Oxide and Angiotensin in the Circulation

“…It seems that nonselective NOS inhibition increases the oxygen costs of kidney function independently of ANG II and that kidney nNOS is responsible for these in vivo and in vitro effects. Solhaug et al (1996a) suggested that NO is vital in the developing kidney to maintain normal physiological function and to protect the immature kidney during pathophysiological stress. Springate et al (1997) noted that mouse renin genetransgenic rats had a blunted pressure-diuresis-natriuresis response that was corrected by inhibition of the renin-ANG system and suggested that their production of NO was normal.…”

Effects of Maternal Renal Dysfunction on Fetal Development

“…In the developing kidney, NO plays an important role in maintaining normal physiological function (Solhaug et al, 1996) and in regulating renal homodynamics . Maintenance of adequate NO is an additional mechanism for the preservation of vasculature in progressive renal diseases (Kang et al, 2002).…”