Previously we showed that neonatal induced chronic partial unilateral ureteral obstruction (PUUO) of the multipapillary pig kidney decreased glomerular filtration rate (GFR) of the obstructed kidney. We hypothesized that angiotensin II (ANG II) and nitric oxide (NO) are important for the changes in renal function and in the present study we examined the effects of chronic AT1 receptor blockade using CV-11974 (candesartan, 0.12 mg/hour from age 23 to 30 days) on kidney function development after PUUO was induced in two-day old piglets. Moreover, the effect of superimposed acute NO inhibition using L-NAME (15 mg/kg) was examined to identify if this has diagnostic potential. PUUO significantly increased GFR in the non-obstructed contralateral kidney independent of candesartan. In candesartan treated piglets the L-NAME induced GFR reduction seen in normal and non-obstructed kidneys was absent in the partial obstructed kidneys. Urine output and fractional excretion of water was increased from the partial obstructed kidneys. Consistent with this immunohistochemical analyses showed a reduced aquaporin-2 (AQP2) labeling in the collecting duct principal cells. Moreover, renal sodium handling was compromised by PUUO evidenced by an increased fractional excretion of sodium (FE_Na) which was enhanced by candesartan treatment. In conclusion, our findings suggest that the counterbalance between AT1 receptor-mediated vasoconstriction and NO-mediated vasodilatation which maintain GFR in normal young porcine kidneys is changed by neonatal induced chronic PUUO. This may have diagnostic potential in children with suspected congenital obstruction. Our results also demonstrate compromised tubular functions in response to chronic PUUO despite preservation of glomerular function.