Angiotensin II injures the arterial wall causing increased aortic stiffening in @entity6970 -deficient XXXX .

@entity6970 @entity101 @entity19 @entity15395 @entity16 @entity1854 @entity439 @entity731 @entity65
@entity65 , such as @entity731 and @entity101 , are associated with arterial stiffening. Previous studies showed that @entity15395 exacerbated @entity731 and induced @entity101 and @entity439 formation in @entity6970 -deficient ( @entity6970 -KO) @entity19 . The aim of the present study was to examine the effects of chronic treatment of @entity15395 on the arterial elastic properties in @entity6970 -KO @entity19 . We hypothesized that @entity15395 will injure the arterial wall resulting in increased arterial stiffening. Male @entity6970 -KO @entity19 were infused with either @entity15395 (1.44 mg. kg(-1). day(-1)) or vehicle (PBS) for 30 days. @entity15395 treatment accelerated @entity731 in the carotid artery by sixfold (P < 0.001) and increased blood pressure by 30% (P < 0.05). Additionally, our data demonstrated that @entity15395 increased arterial stiffening using both in vivo and in vitro methods. @entity15395 significantly increased pulse wave velocity by 36% (P < 0.01) and decreased arterial elasticity as demonstrated by a more than 900% increase in maximal stiffening (high strain Young's modulus) compared with vehicle (P < 0.05). These functional changes were correlated with morphological and biochemical changes as demonstrated by an increase in collagen content (60%), a decrease in elastin content (74%), and breaks in the internal elastic lamina in the aortic wall. In addition, endothelium-independent vasorelaxation to @entity1854 was impaired in the aortic rings of @entity15395 -treated @entity19 compared with vehicle. Thus, the present data indicate that @entity15395 injures the artery wall in multiple ways and arterial stiffening may be a common outcome of @entity15395 -induced @entity16 .
