Objective: Fawn-Hooded (FH) rat strain represents unique model of hypertension with renal failure. Normotensive FHL rats serve as a control whereas FHH develop early hypertension and exhibit increased susceptibility to renal disease due to impaired autoregulatory efficiency of the kidney. Aim of this study was to examine the influence of nitric oxide (NO) system in FHL and FHH rats in prehypertensive and hypertensive period. Design and method: 3 and 9 months old FHH and FHL rats were anesthetized, NO synthase inhibitor (L-NAME) were infused via jugular vein in dose 50 μg/kg of body weight and mean arterial pressure (MAP), renal blood flow (RBF), glomerular filtration rate (GFR), urine flow (UF) and sodium excretion responses were measured. Results: FHH rats exhibited significantly higher basal MAP compare to FHL in 3 month (123 ± 2,9 vs. 101 ± 2,5 mmHg) and also in 9 month (141 ± 2,1 vs. 102 ± 2,4 mmHg). Young FHH had higher basal RBF than FHL (6,5 ± 0,2 vs. 5,4 ± 0,5 ml/min/g) although older FHH rats had slightly lower RBF compare to FHL (3,7 ± 0,5 vs. 4,9 ± 0,5 ml/min/g) and also GFR (0,47 ± 0,07 vs. 0,66 ± 0,09 ml/min/g). L-NAME administration led to similar responses in both ages in MAP, RBF and GFR but hypertensive FHH had significantly lower increase in UF (from 3,7 ± 0,4 to 13,6 ± 2,5 µl/min/g) compare to FHL (from 4,4 ± 0,8 to 29,7 ± 2,6 µl/min/g) and also in sodium excretion (from 0,19 ± 0,07 to 1,57 ± 0,54 µmol/min/g) than in FHL (from 0,14 ± 0,08 to 3,77 ± 0,57 µmol/min/g). Conclusions: This study indicates that FHH rats with developed hypertension exhibit impaired renal hemodynamics and tubular function that may be caused by relative NO deficiency in the kidney.