Analysis Tools
cardiovascular system
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• homozygotes show a 56% reduction in the L-type calcium channel population of aortic smooth muscle membranes, as shown by dihydropyridine binding studies
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• in response to a high salt diet (8% NaCl; 3 months), homozygotes exhibit hypertrophy of the aortic smooth muscle layer
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• in response to a high salt diet (8% NaCl; 3 months), homozygotes develop cardiac enlargement
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• on a high salt diet (8% NaCl; 3 months), homozygotes exhibit a significantly increased heart weight relative to wild-type mice
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• on a normal diet, 12-16-wk-old homozygotes show no significant differences in systolic or diastolic blood pressure relative to wild-type mice
• however, i.p. injection of amlodipine, a DHP analog, fails to reduce systolic and diastolic blood pressure in mutant mice
• on a high salt diet (8% NaCl; 2 weeks), homozygotes (but not wild-type mice) exhibit elevated blood pressure and subsequent hypertrophic changes, in the absence of altered kidney morphology or plasma renin concentrations
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• on a high salt diet (8% NaCl; 2 weeks), homozygotes (but not wild-type mice) show increased diastolic blood pressure
• however, i.p. injection of amlodipine fails to cause the expected reduction in diastolic blood pressure
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• on a high salt diet (8% NaCl; 2 weeks), homozygotes (but not wild-type mice) show increased systolic blood pressure
• however, i.p. injection of amlodipine fails to cause the expected reduction in systolic blood pressure
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• homozygotes display a congenital 30% reduction in Ca2+ channel current density, a slower inactivation rate, and a reduced dihydropyridine (DHP)-sensitive current in aortic smooth muscle cells
• in response to KCl, homozygotes show reduced responsiveness to diltiazem (an L-type calcium channel blocker) in the global [Ca2+]i, with no significant changes in local Ca2+ sparks in mesenteric arteries
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muscle
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• homozygotes show a 56% reduction in the L-type calcium channel population of aortic smooth muscle membranes, as shown by dihydropyridine binding studies
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|
• in response to a high salt diet (8% NaCl; 3 months), homozygotes exhibit hypertrophy of the aortic smooth muscle layer
|
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• homozygotes display a congenital 30% reduction in Ca2+ channel current density, a slower inactivation rate, and a reduced dihydropyridine (DHP)-sensitive current in aortic smooth muscle cells
• in response to KCl, homozygotes show reduced responsiveness to diltiazem (an L-type calcium channel blocker) in the global [Ca2+]i, with no significant changes in local Ca2+ sparks in mesenteric arteries
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immune system
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• initial peak and plateau calcium responses are attenuated compared to in wild-type mice
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• IL-4 production is reduced
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homeostasis/metabolism
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• homozygotes display a congenital 30% reduction in Ca2+ channel current density, a slower inactivation rate, and a reduced dihydropyridine (DHP)-sensitive current in aortic smooth muscle cells
• in response to KCl, homozygotes show reduced responsiveness to diltiazem (an L-type calcium channel blocker) in the global [Ca2+]i, with no significant changes in local Ca2+ sparks in mesenteric arteries
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hematopoietic system
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• initial peak and plateau calcium responses are attenuated compared to in wild-type mice
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growth/size/body
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• in response to a high salt diet (8% NaCl; 3 months), homozygotes develop cardiac enlargement
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• on a high salt diet (8% NaCl; 3 months), homozygotes exhibit a significantly increased heart weight relative to wild-type mice
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