Myocardial hypertrophy in the absence of external stimuli is induced by angiogenesis in mice
J. Clin. Invest. Daniela Tirziu, et al. 117:3188 doi:10.1172/JCI32024 [
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Figure 6Cardiac hypertrophy reduction after
l-NAME treatment.
(
A) Cycle GMP production in
tTA+/PR39+ and control mouse hearts after 6 weeks of PR39 induction (
n = 4 mice/group). (
B) Heart weight measurements after 6 weeks of PR39 induction with and without
l-NAME treatment (0.5 g/l tap water).
l-NAME was given during the last 3 weeks of a 6-week induction period. Note reduction of the increase in heart size caused by PR39 induction (untreated,
n = 16 mice/group;
l-NAME treated,
n = 12 mice/group). (
C) RT-PCR analysis of hypertrophy marker expressions in
l-NAME–treated versus untreated mice. GAPDH expression used as control. Representative data are shown. Note reduced expression of hypertrophic markers in
l-NAME–treated mice. (
D) Capillary mass of
l-NAME–treated versus untreated mice. (
E) Western blot analysis of expression of caveolin-1 (normalized to VE-cadherin) and caveolin-3 (normalized to skeletal α–actinin) after 6 weeks of PR39 induction in the absence or presence of
l-NAME (
n = 3 mice/group). Note caveolin-1 and -3 expression restoration by
l-NAME treatment. (
F and
G) Effect of
l-NAME treatment on LV function. Echocardiographic assessment of posterior wall thickness in diastole in
F and LV end-systolic dimension in
G. Untreated,
n = 15 mice/group;
l-NAME treated,
n = 6 mice/group. **
P < 0.001; *
P < 0.05.
