Analysis Tools
cardiovascular system
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• moderate hypertrophy of the small renal arteries is observed
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• in 12 month old males, heart weight is increased compared to in wild-type male mice
• however, no evidence of cardiac hypertrophy is detected
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• left ventricle end-diastolic diameter normalized to body weight is increased (0.17+/-0.01 compared to 0.15+/-0.01 in wild-type mice)
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• mice display progressive cardiac fibrosis without cardiomyocyte hypertrophy or inflammation
• at 4 months, fibrosis is primarily found in the pericoronary area with some evident in the interstitial spaces
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• at 4 months, fibrosis is primarily found in the pericoronary area with some evident in the interstitial spaces
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• at 12 months, abnormal diastolic function is accompanied by high left ventricle filling pressure (depicted by the ratio of maximal velocity of early left ventricle inflow to the maximal velocity of early diastolic motion of the mitral annulus, with relative conservation of systolic function)
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• as early as 5 weeks, mice exhibit an increase of about 20 mmHg in systolic blood pressure compared to wild-type mice that is more severe in males than females and persists with similar severity throughout life without progressive aggravation
• following exposure to angiotensin II, blood pressure plateaus for at least 30 minutes after initial rise without returning to basal levels as in wild-type mice
• following cumulative doses of angiotensin II, systolic blood pressure after 10 minutes rises to 60 mmHg compared to 25 mmHg in wild-type mice
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homeostasis/metabolism
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• creatinine excretion is reduced relative to in wild-type mice
• however, plasma creatinine levels are normal
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• plasma urea levels are increased (8.7+/-0.4 mmol/l compared to 7.1+/-0.5 mmol/l)
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• immunoreactive angiotensin plasma concentration is decreased by 50% compared to wild-type mice; unclear whether this decrease involves Ang II, Ang III, and Ang IV equally
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• potassium concentration in the urine is reduced (333+/-31 umol/d compared to 433+/-33 umol/d in wild-type mice)
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• urine osmolarity is increased (2504+/-166 mOsm/kg water compared to 2044+/-101 mOsm/kg water in wild-type mice)
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• while mice are responsive to candesartan, losartan treatment does not reduce blood pressure
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renal/urinary system
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• moderate hypertrophy of the small renal arteries is observed
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• creatinine excretion is reduced relative to in wild-type mice
• however, plasma creatinine levels are normal
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• potassium concentration in the urine is reduced (333+/-31 umol/d compared to 433+/-33 umol/d in wild-type mice)
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• urine osmolarity is increased (2504+/-166 mOsm/kg water compared to 2044+/-101 mOsm/kg water in wild-type mice)
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• periglomerular and perivascular fibrosis is observed in the kidney
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• mice output less urine (1.09+/-0.13 ml compared to 1.50+/-0.11 ml in wild-type mice)
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hematopoietic system
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• mice have 17% more red blood cells than wild-type mice
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• mice have 12% more hemoglobin than wild-type mice
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growth/size/body
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• in 12 month old males, heart weight is increased compared to in wild-type male mice
• however, no evidence of cardiac hypertrophy is detected
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• beginning at 1 to 3 months, mice weight 10% to 20% less than wild-type mice
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cellular
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• at 4 months, fibrosis is primarily found in the pericoronary area with some evident in the interstitial spaces
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