Abstract
Similar sets of changes were observed in the myocardium during physiological aging and long-term cardiac hyperfunction: RNA concentrations decreased, rates of RNA and protein synthesis dropped, while the rates of RNA and protein degradation decreased as well. The rates of protein synthesis and degradation in the myocardium of old rats and rats with prolonged compensatory cardiac hypertrophy (CCH) decreased to the same extent when compared with young rats. The decrease in the rate of protein synthesis in both cases resulted from at least two factors: (1) a fall in ribosome concentrations in the tissue of the myocardium, and (2) a diminution in the rate of translation owing to tRNA deficiency. The rate of RNA synthesis and degradation in the myocardium of rats with CCH decreased to a greater extent than in the myocardium of old rats under normal physiological conditions. It is concluded that long-term cardiac hyperfunction and hypertrophy speeds up the natural aging of the myocardium, a decrease in the rate of turnover of RNA and proteins being the driving force in this process.
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