renal/urinary system
• following unilateral ureter obstruction, mice exhibit increased kidney size, distended renal tissue, unclear border between the outer and inner medulla, severe hydronephrosis, and smaller medulla to cortex ratio compared with similarly treated wild-type mice
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• following unilateral ureter obstruction compared with similarly treated wild-type mice
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• more severe following unilateral ureter obstruction compared to in similarly treated wild-type mice
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homeostasis/metabolism
• following unilateral ureter obstruction, mice exhibit increased kidney size, distended renal tissue, unclear border between the outer and inner medulla, severe hydronephrosis, and smaller medulla to cortex ratio compared with similarly treated wild-type mice
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cardiovascular system
N |
• mice exhibit normal blood pressure and heart rate
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• mutants exhibit adverse aortic remodeling after 2 weeks of angiotensin II infusion compared to wild-type mice, showing disorganized and disrupted elastin fibers and disorganized collagen structures, especially in the abdominal aorta
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• angiotensin II infused mutants exhibit disrupted medial elastic lamellae and fibrillar structures in the abdominal aortic walls
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• mutants treated with angiotensin II exhibit an increase in macrophage infiltration in the abdominal aorta and disrupted medial elastic lamellae and fibrillar structures in the abdominal aortic walls
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• 60% of mutants develop abdominal aortic aneurysm after 4 weeks of angiotensin II infusion unlike wild-type mice, showing greater than 50% aortic dilation in the suprarenal region
• treatment with a broad spectrum protease inhibitor, PD166793, during the course of angiotensin II infusion blocks abdominal aortic aneurysm development
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• the aortic systolic expansion index, a measure of aortic elasticity and recoil property during systole and diastole is suppressed in the aneurysmal aorta of angiotensin II infused mutants
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• mutants treated with angiotensin II exhibit an increase in macrophage infiltration in the abdominal aorta
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immune system
• mutants treated with angiotensin II exhibit an increase in macrophage infiltration in the abdominal aorta
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mortality/aging
• survival is compromised after angiotensin II infusion due to aortic rupture, with mice showing 80-85% survival 28 days after infusion
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growth/size/body
• following unilateral ureter obstruction compared with similarly treated wild-type mice
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