Role of intrarenal angiotensin system activation, oxidative stress, @entity32 , and impaired XXXX activity in the progression of @entity628 .

@entity407 @entity644 @entity8 @entity32 @entity101 @entity4988 @entity628 @entity1808 @entity1110 @entity177 @entity2629 @entity4027 @entity9885 @entity35 @entity631
The Imai @entity35 is a model of spontaneous @entity628 , which leads to heavy @entity644 , @entity407 , @entity101 , and progressive @entity177 . Treatment with AT1 blockers (ARBs) ameliorates @entity644 , @entity407 , and @entity8 in this model. Progression of @entity8 in 5/6 nephrectomized @entity35 is associated with activation of the intrarenal angiotensin system, up-regulation of the oxidative, inflammatory, and fibrogenic pathways, and impaired activity of @entity4027 ( @entity4027 ), the master regulator of genes encoding antioxidant molecules. We hypothesized that progressive @entity8 in the Imai @entity35 is accompanied by oxidative stress, @entity32 , and impaired @entity4027 activation and that amelioration of @entity8 with AT1 receptor blockade in this model may be associated with the reversal of these abnormalities. Ten-week-old Imai @entity35 were randomized to the ARB-treated ( @entity9885 , 10 mg/kg/day for 24 weeks) or vehicle-treated groups. @entity35 served as controls. At 34 weeks of age Imai @entity35 showed heavy @entity644 , @entity4988 , @entity101 , @entity2629 , @entity631 , @entity32 , increased @entity1808 expressing cell population, up-regulations of AT1 receptor, AT2 receptor, @entity1110 oxidase, and inflammatory mediators, activation of nuclear factor-kB and reduction of @entity4027 activity and expression of its downstream gene products in the renal cortex. ARB therapy prevented @entity8 , suppressed oxidative stress and @entity32 , and restored @entity4027 activation and expression of the antioxidant enzymes. Thus progressive @entity628 in the Imai @entity35 is associated with oxidative stress, @entity32 , and impaired @entity4027 activation. These abnormalities are accompanied by activation of intrarenal angiotensin system and can be prevented by ARB administration.
