Analysis Tools
mortality/aging
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• 3 of 14 mutant mice, but no wild-type mice, die during angiotensin II infusion (1.2 mg/kg) due to ruptured abdominal aortic aneurysms
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cardiovascular system
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• at baseline, untreated mutant mice show slightly larger (5%) abdominal aortic artery diameters than wild-type mice
• after angiotensin II infusion, mutant mice show dose-dependent increases in abdominal aortic diameters, unlike similarly treated wild-type mice
• after day 4 of high-dose angiotensin II infusion (2.4 mg/kg), mutant abdominal aortic diameters continue to enlarge, whereas those of wild-type mice remain unchanged
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• cardiac mitochondria are 5% more eccentric than mitochondria from wild-type mice
• however, crista structure is normal
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• mutant mice exhibit normal left ventricle (LV) dimensions and fractional shortening but develop isolated left atrial (LA) enlargement at 16 to 18 months of age (20% increased LA diameter)
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• 3 of 14 mutant mice, but no wild-type mice, die during angiotensin II infusion (1.2 mg/kg) due to ruptured abdominal aortic aneurysms
• however, no aortic aneurysms or ruptures occur following norepinephrine-induced hypertension
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• after 2 weeks of angiotensin II infusion, mutant mice exhibit significantly decreased fractional shortening in comparison with baseline, unlike similarly treated wild-type mice; however, LV dimensions remain normal
• infusion of low or high doses of angiotensin II show dose-dependent but equivalent increases in systolic blood pressure in both mutant and wild-type mice
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• single cardiomyocytes from mutant mice (ages 6 to 8 weeks) exhibit slower relaxation rates than wild-type cardiomyocytes
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• single cardiomyocytes from mutant mice (ages 6 to 8 weeks) exhibit delayed sarcomere relaxation and cytosolic calcium reuptake kinetics, indicating diastolic dysfunction
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• single cardiomyocytes from mutant mice (ages 6 to 8 weeks) exhibit slower repolarization kinetics, as shown by both decreased sarcomere relaxation velocity and increased time constant (Tau), for calcium reuptake
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cellular
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• cardiac mitochondria are 5% more eccentric than mitochondria from wild-type mice
• however, crista structure is normal
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• cardiac mitochondria are 20% smaller than mitochondria from wild-type mice
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• liver mitochondria isolated from mutant mice take up Ca2+ slower at high [Ca2+] and faster at low [Ca2+] relative to wild-type liver mitochondria
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muscle
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• cardiac mitochondria are 5% more eccentric than mitochondria from wild-type mice
• however, crista structure is normal
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• after 2 weeks of angiotensin II infusion, mutant mice exhibit significantly decreased fractional shortening in comparison with baseline, unlike similarly treated wild-type mice; however, LV dimensions remain normal
• infusion of low or high doses of angiotensin II show dose-dependent but equivalent increases in systolic blood pressure in both mutant and wild-type mice
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• single cardiomyocytes from mutant mice (ages 6 to 8 weeks) exhibit slower relaxation rates than wild-type cardiomyocytes
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