Analysis Tools
cardiovascular system
hypertension
(
J:274218
)
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• mice exhibit higher blood pressure at 8 weeks of age
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homeostasis/metabolism
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• mice fed a high-potassium diet develop hypokalemia as in wild-type mice but plasma potassium levels are higher than in wild-type mice
• potassium gavage causes a higher rise in plasma potassium concentration than in wild-type mice
• while plasma potassium levels do decrease after feeding a potassium-deficient diet, levels remain higher than in wild-type mice
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hyperkalemia
(
J:274218
)
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• plasma potassium concentration is increased
|
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• lower total carbon dioxide levels
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• fractional excretion of potassium is lower, and this together with increased plasma potassium levels indicates that tubular potassium secretion is impaired
• however, mice show normal stead-state urinary potassium excretion rate
• mice fed a potassium-deficient diet show a slightly, but significant, slower rate of decrease of urinary potassium excretion
• the urinary fractional excretion of potassium (reflecting tubular potassium excretory ability) remains depressed in mutants fed a potassium-deficient diet
|
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• mice fed a high-potassium diet exhibit a higher urinary potassium excretion rate in the first 0-24 hours of the diet compared to wild-type mice but remains similar to wild-type mice during days 2-4 of the diet
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• mice show a lower amiloride-sensitive urinary sodium excretion rate than wild-type mice
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• on a potassium-deficient diet, sodium excretion remains stable compared to a gradual decline in wild-type mice
• mice fed a high-potassium diet show a similar increase in urinary sodium excretion within 6 hours of the diet and this natriuresis partially subsides, but remains at a level higher than 2-fold of controls
• mice show a higher thiazide-sensitive urinary sodium excretion rate than wild-type mice
• a potassium-deficient diet does not further increase thiazinde-sensitive urinary sodium excretion rate
• however, mice show normal urinary sodium excretion rate in the steady state
|
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• hyperchloremic metabolic acidosis
• however, blood pH is normal
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renal/urinary system
|
• fractional excretion of potassium is lower, and this together with increased plasma potassium levels indicates that tubular potassium secretion is impaired
• however, mice show normal stead-state urinary potassium excretion rate
• mice fed a potassium-deficient diet show a slightly, but significant, slower rate of decrease of urinary potassium excretion
• the urinary fractional excretion of potassium (reflecting tubular potassium excretory ability) remains depressed in mutants fed a potassium-deficient diet
|
|
• mice fed a high-potassium diet exhibit a higher urinary potassium excretion rate in the first 0-24 hours of the diet compared to wild-type mice but remains similar to wild-type mice during days 2-4 of the diet
|
|
• mice show a lower amiloride-sensitive urinary sodium excretion rate than wild-type mice
|
|
• on a potassium-deficient diet, sodium excretion remains stable compared to a gradual decline in wild-type mice
• mice fed a high-potassium diet show a similar increase in urinary sodium excretion within 6 hours of the diet and this natriuresis partially subsides, but remains at a level higher than 2-fold of controls
• mice show a higher thiazide-sensitive urinary sodium excretion rate than wild-type mice
• a potassium-deficient diet does not further increase thiazinde-sensitive urinary sodium excretion rate
• however, mice show normal urinary sodium excretion rate in the steady state
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| pseudohypoaldosteronism | DOID:4479 | J:274218 | ||
