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J Am Coll Cardiol, 2004; 44:1320-1327, doi:10.1016/j.jacc.2004.06.030
© 2004 by the American College of Cardiology Foundation
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Physical inactivity causes endothelial dysfunction in healthy young mice

Tatsiana Suvorava, PhD, Nadine Lauer, PharmD, PhD and Georg Kojda, PharmD, PhD*

Institut fuer Pharmakologie und Klinische Pharmakologie, Heinrich-Heine-Universitaet, Duesseldorf, Germany



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Figure 1 Details of the cages used to house mice in groups (bottom cage) and singularized mice (top cage).

 


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Figure 2 Activity of citrate synthase in homogenates of soleus (A, B) and cardiac left ventricular muscle (C, D) of singularized mice (sedentary, n = 7, all panels), mice living in groups (moving, n = 5) (A, C) and singularized mice that underwent three weeks of endurance training (exercise, n = 7) (B, D) (*p < 0.05, unpaired two-tailed Student t test).

 


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Figure 3 Endothelium-dependent vasodilation in aortic rings of sedentary mice after (A) five weeks of singularization (n = 6) compared with mice living in groups of five animals per cage (moving mice, n = 6) and (B) after nine weeks of singularization (n = 7) compared with moving mice (n = 5) and with sedentary (n = 7) and moving mice (n = 5) that underwent the exercise program. Physical inactivity induced by singularization resulted in a significant impairment of endothelium-dependent vasorelaxation (* = p < 0.001, analysis of variance). Three weeks of exercise completely reversed this impairment, whereas exercise training had no effect on endothelium-dependent vasodilation in moving mice.

 


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Figure 4 Vasoconstrictor response to increasing concentrations of phenylephrine in aortic rings of singularized sedentary mice (n = 6) and moving mice (n = 6). There was no difference between the groups (p = 0.6262, analysis of variance).

 


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Figure 5 Vasodilator response to increasing concentrations of the nitric oxide donor racemic S-nitroso-N-acetylpenicillamine in aortic rings of singularized sedentary mice (n = 6) and of moving mice (n = 6). There was no difference between the groups (p = 0.4059, analysis of variance).

 


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Figure 6 (A) Protein expression of eNOS in aortic rings of singularized sedentary mice (n = 5) compared with moving mice (n = 5) and (B) of moving mice (n = 4) compared with moving mice that underwent an exercise program (n = 4). Singularization resulted in a significant reduction of eNOS protein expression (A, p < 0.01), whereas exercise had no effect on eNOS protein expression in moving mice (B, p > 0.05, unpaired two-tailed Student t test).

 


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Figure 7 Effect of 8 days (n = 5) and 15 days of exercise (n = 5) on eNOS-protein expression in (A) aortic rings and (B) left ventricular myocardium of singularized sedentary mice (n = 5 for each exercise period). Although exercise induced a significant and time-dependent upregulation of eNOS protein expression in aortic rings (p = 0.0147, analysis of variance), there was only a trend in left ventricular myocardium (p = 0.1637). Subsequent Newman-Keuls multiple comparison test of the data depicted in A revealed a significant difference only for the comparison sedentary versus 15 days' exercise as indicated (*, p < 0.05, analysis of variance).

 




 
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