Abstract
Summary
The biochemical mechanism by which increased heart tension results in cardiac hypertrophy is unknown. In vitro studies using muscle cell cultures have suggested that the concentration of creatine is the chemical mediator of this hypertrophy. To examine this mechanism in vivo, the myocardial concentration of ATP, CP and Cr was serially measured following aortic constriction. The aortic constriction resulted in a 53% increase in heart weight after 2 weeks. The concentration of ATP, CP or Cr decreased following aortic constriction to a level 20-50% below control values. These data suggest that the creatine concentration in vivo is not the stimulus for hypertrophy, but the decreased creatine concentration in hypertrophied hearts may limit the level of ATP and CP that can be maintained during the development of cardiac hypertrophy.
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