ACE inhibition (ACEi) ameliorates the development of hypertension and the intrarenal Ang II augmentation in Ang II-infused mice. To determine if these effects are associated with changes in the mouse intrarenal RAS, the expression of angiotensinogen (AGT), renin, ACE, AT₁R mRNA (by qRT-PCR) and protein (by Western blot -WB- and/or immunohistochemistry -IHC-) were analyzed. Nine-12 week C57BL/6J male mice were distributed as controls (n=10), Ang II-infused (Ang II=8, 400 ng/kg/min for 12 d), ACEi only (ACEi=10, lisinopril, 100 mg/L) and Ang II-infused + ACEi (Ang II+ACEi=11). When compared to controls (1.00), AGT protein (by WB) was increased by Ang II (1.29±0.13, p<0.05), and this was not prevented by ACEi (ACEi+Ang II, 1.31±0.14, p<0.05). ACE protein (by WB) was increased by Ang II (1.21±0.08, p<0.05) and it was reduced by ACEi alone (0.88±0.07, p<0.05) or in combination with Ang II (0.80±0.07, p<0.05). AT₁R protein (by WB) was increased by Ang II (1.27±0.06, p<0.05) and ACEi (1.17±0.06, p<0.05) but not Ang II+ACEi (1.15±0.06, NS). Tubular renin protein (semi-quantified by IHC) was increased by Ang II (1.49±0.23, p<0.05) and ACEi (1.57±0.15, p<0.05), but not Ang II+ACEi (1.10±0.15, NS). No significant changes were observed in AGT, ACE or AT₁R mRNA. In summary, reduced responses of intrarenal tubular renin, ACE, and the AT₁R protein to the stimulatory effects of chronic Ang II infusions, in the presence of ACEi, are associated with the effects of this treatment to ameliorate augmentations in blood pressure and intrarenal Ang II content during Ang II-induced hypertension.