This study was performed to test the hypothesis that angiotensin II (Ang II) contributes to the hypertension and renal functional alterations induced by a decrease of COX2 activity during nephrogenic period. It was also examined whether renal functional reserve and renal response to volume overload and high sodium intake are reduced in 3-4 and 9-11 months old male and female rats treated with vehicle or a COX2 inhibitor during nephrogenic period (COX2np). Our data show that this COX2 inhibition induces an Ang II-dependent hypertension that is similar in male and female rats. Renal functional reserve is reduced in COX2np-treated rats since their renal response to an increase in plasma aminoacids levels is abolished, and their renal ability to eliminate a sodium load is impaired (P<0.05). This reduction in renal excretory ability is similar in both sexes during aging but does not induce the development of a sodium-sensitive hypertension. However, the prolonged high sodium intake at 9-11 months of age leads to a greater proteinuria in male than in female (114±12 mg/min vs. 72±8 mg/min, P<0.05) COX2np-treated rats. Renal hemodynamic sensitivity to acute increments in Ang II is unaltered in both sexes and at both ages in COX2np-treated rats. In summary, these results indicate that the reduction of COX2 activity during nephrogenic period programs for the development of an Ang II-dependent hypertension, reduces renal functional reserve to a similar extent in both sexes, and increases proteinuria in males but not in females when there is a prolonged increment in sodium intake.