growth/size/body
• mutant mice fed a high K+ (5% KCl) diet for 3 days show a significantly increased body weight on HK day 2, unlike wild-type controls where increased K+ intake has no effect on body weight
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cardiovascular system
• mutant mice fed a high K+ (5% KCl) diet display significantly increased systolic BP and remain hypertensive for 3 days during increased K+ intake, unlike wild-type controls
• addition of amiloride (an epithelial Na+ channel inhibitor) in drinking water abolishes high K+ intake-induced hypertension and decreases systolic BP from 146 +/- 5 to 117 +/- 3 mmHg, unlike in wild-type controls where amiloride has no effect on BP
• mutant mice fed a high-salt (4% NaCl) diet for 3 days show no significant differences in mean systolic BP relative to wild-type controls
• no differences in mean systolic BP are observed under normal salt or normal K+ (1.0% KCl) conditions relative to wild-type controls
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renal/urinary system
• mutant mice fed a high K+ (5% KCl) diet display significantly decreased Na+ excretion relative to mutant mice fed a normal K+ (1.0% KCl) diet, unlike wild-type controls
• however, mutant mice exhibit no differences in Na+ intake when fed a 5% KCl diet or a normal (1.0% KCl) diet
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• 10 uM of arachidonic acid (AA) fails to inhibit apical epithelial Na+ channel (ENaC) activity in the cortical collecting duct (CCD) of mutant mice fed a high K+ (5% KCl) diet, unlike in wild-type controls where channel activity (NPo) is decreased from 1.2 +/- 0.2 to 0.3 +/- 0.1
• however, addition of 100 nM 11,12-epoxyeicosatrienoic acid (11,12-EET) is still able to inhibit ENaC in the CCD of mutant mice fed a high K+ (5% KCl) diet, with NPo reduced from 2.5 +/- 0.4 to 0.2 +/- 0.1
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homeostasis/metabolism
• mutant mice fed a high K+ (5% KCl) diet display significantly decreased Na+ excretion relative to mutant mice fed a normal K+ (1.0% KCl) diet, unlike wild-type controls
• however, mutant mice exhibit no differences in Na+ intake when fed a 5% KCl diet or a normal (1.0% KCl) diet
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