Deletion of inducible nitric oxide synthase provides cardioprotection in XXXX with 2-kidney, 1-clip @entity101 .

@entity101 @entity1184 @entity19 @entity3542 @entity409 @entity1283 @entity1507 @entity18511 @entity4346 @entity13633 @entity3044 @entity11838
@entity13633 ( @entity13633 ) has been implicated in the pathogenesis of @entity101 and target organ damage. We hypothesized that induction of @entity13633 contributes to left ventricular (LV) @entity1184 and @entity409 in @entity19 with 2-kidney, 1-clip @entity101 . Deletion of @entity13633 diminishes oxidative stress, thereby attenuating @entity4346 and enhancing cardiac performance. 2-Kidney, 1-clip @entity101 was induced in @entity19 lacking @entity13633 and wild-type controls (C57BL/6J). Sham-clipped @entity19 served as controls. Systolic blood pressure was measured weekly by tail cuff. Left ventricular ejection fraction (by echocardiography) and cardiac response (maximum and minimum dP/dt, as well as an indicator of isovolumic contraction) to @entity3044 (50 ng per @entity19 , i.v.) were studied at the end of the experiment. @entity11838 (a byproduct of lipid peroxidation and an indicator of oxidative stress) was measured by immunohistochemical staining. @entity18511 (phox), endothelial NO synthase, and @entity13633 protein expression were determined by Western blot. We found that systolic blood pressure, LV weight, myocyte cross-sectional area, interstitial collagen fraction, ejection fraction, and cardiac response to @entity3044 did not differ between strains with sham clipping. 2-Kidney, 1-clip @entity101 increased systolic blood pressure, LV weight, myocyte cross-sectional area, and interstitial collagen fraction similarly in both strains. However, in @entity19 lacking @entity13633 , maximum and minimum dP/dt, as well as an indicator of isovolumic contraction, markedly increased in response to @entity3044 , associated with decreased cardiac @entity11838 expression and urinary @entity1507 / @entity3542 . We concluded that deletion of @entity13633 does not seem to play a significant role in preventing 2-kidney, 1-clip @entity101 -induced @entity101 and @entity1283 ; however, it does enhance preservation of cardiac function, probably because of a reduction of @entity13633 -induced oxidative stress.
