It has been previously reported that the Wistar-Furth (WF) rats are protected against chronic renal failure induced by several models, showing preserved renal nitric oxide (NO) production compared to control rats. In the present study, our aim was to evaluate the morpho-functional responses to renal ischemia-reperfusion (IR) in WF and Wistar-Hanover (WH) rats. To do so, we analysed the temporal evolution of renal function, oxidative stress and inflammation. Renal excretory capacities were evaluated throughout a 14-days period post-IR in conscious rats placed in metabolic cages. Inflammation was assessed by measuring intrarenal monocyte-chemoattractant protein-1 (MCP-1) levels at different time-points after IR, in correlation with immunostaining of ED1-positive cells. Oxidative stress markers were measured in urine, i.e. hydrogen peroxide (H₂O₂), malonedialdehyde (MDA), as well as NO metabolites (NOx). Our results indicated that the increase in urine output, associated with a lowered osmolarity observed during the first 5 days post-IR, were more pronounced in WF rats, compared to WH rats. Simultaneously, the early increase in urinary excretion of NGAL, a new biomarker of renal injury, was attenuated in WF rats. Intrarenal MCP-1 levels were characterized by significant peak values at 24h post-IR, with no difference between the two strains, while the interstitial accumulation of ED1-positive cells was maximal at day 7. As for oxidative stress, H₂O₂ and MDA urinary excretion rates were significantly enhanced as soon as 24h post-IR, and thereafter returned towards baseline at day 7, with a similar temporal pattern in both strains. NOx urinary excretion rates were similarly decreased in WF and WH rats at 48h post-IR and returned to baseline at day 7. In summary, these preliminary results seem to indicate that the functional difference observed between WF and WH rats could not be related to differences in NO production, nor inflammation or oxidative stress, and therefore need to be further investigated.