ROLE OF NITRIC-OXIDE IN THE HYPOXEMIA-INDUCED RENAL DYSFUNCTION OF THE NEWBORN RABBIT

The current study was performed in 30 anesthetized and mechanically ve ntilated newborn rabbits to investigate the role of the endothelium-de rived relaxing factor nitric oxide (NO) in the renal vasoconstriction observed during hypoxemia. Renal blood flow (RBF) and GFR were determi ned by the clearance of p-aminohippuric acid and inulin, respectively. In nine newborn rabbits (group 1), acute hypoxemia induced a signific ant decrease in RBF (-17 +/- 7%) and GFR (-11 +/- 6%). A second group of nine animals was used to determine the role of NO in regulating ren al hemodynamics of the immature kidney in physiologic conditions. N-om ega-Nitro-L-arginine methyl ester (L-NAME), a NO synthesis inhibitor, significantly increased the renal vascular resistance by 31 +/- 9% and decreased RBF and GFR (-20 +/- 6% and -13 +/- 5%, respectively). Acut e hypoxemia was induced in 12 additional newborn rabbits during L-NAME infusion (group 3) to define the role of NO in the renal vasoconstric tion observed during hypoxemia. The changes in renal hemodynamics were greater in this group than in those induced by hypoxemia alone. The p resent results suggest that: 1) endogenous NO has a crucial role in ma intaining basal renal perfusion, 2) the activity of NO synthase is mai ntained during acute hypoxemia, and 3) NO could blunt the effects of a cute hypoxemia in the immature newborn rabbit kidney.