Physiological and Biochemical Properties of Contractile Protein ATPase Activity of Aging Myocardium
Many regulatory functions in the myocardial cell are changed as a result of age. Growing evidence indicates a significant positive correlation between heart contractile protein enzymatic activity and the functional contractile level of the ventricle. A decrease in myofibrillar, myosin and actomyosin ATPase activity is associated with the aging myocardium (1–3). At high Ca2+ concentrations, the ATPase activity of older rats is significantly lower than that of younger rats. The difference in age-related decline in Ca2+ sensitivity of myocardial ATPase activity may be due to diminished ability of older animals to remove the inhibition of actomyosin ATPase activity by the troponin + tropomyosin system (4). Age-associated alterations in myocardial ultrastructure, cardiac function, excitation-contraction coupling and metabolism have been discussed by several investigators (5,6). Hemodynamic measurements, such as heart rate, cardiac output, blood pressure, and related vascular parameters, have been found in change during the life span of the rat, thus causing the cardiovascular system to operate less efficiently in the older animal (7–9). Cardiac hypertrophy is a characteristic feature that occurs during senescence. It has been shown that depressed contractile protein ATPase activity is a characteristic feature associated with hypertrophy and senescent rat hearts (10–12). Previous reports (13,14) from this laboratory showed that the phosphorylation of contractile proteins is associated with a decrease in contractile protein ATPase activity. The purpose of this study is to investigate age-associated alterations in contractile protein ATPase activity and examine the possible mechanisms associated with such change.
KeywordsDepression EDTA Fluoride Respiration Electrophoresis
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