Contractile proteins and sarcoplasmic reticulum in physiologic cardiac hypertrophy.
To study effects of physiologic hypertrophy on contractile protein ATPases and sarcoplasmic reticulum, hypertrophy was caused in female Wistar rats by a chronic swimming program. Nonhypertrophied hearts of female control sedentary rats and rats made to run on a treadmill program were also examined. The swimming program, but not the running program, resulted in a significant increase in heart weight. Actomyosin ATPase activity was also increased by 15% in the hearts of swimmers but not runners. Similar increases were observed for Ca2+-activated myosin ATPase activity and actin-activated ATPase of myosin. Sarcoplasmic reticulum from the hearts of swimmers showed increased calcium binding and calcium uptake as a function of time and of calcium concentration. Sarcoplasmic reticulum ATPase activities were not altered by hypertrophy. These findings in physiologic hypertrophy contrast with those of pathologic hypertrophy in which ATPase activity of contractile proteins and calcium binding and uptake of sarcoplasmic reticulum have generally been found to be depressed.
D000205:Actomyosin / Q000378:metabolism; D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D001835:Body Weight; D002118:Calcium / Q000378:metabolism; D006332:Cardiomegaly / Q000503:physiopathology*; D004586:Electrophoresis; D005260:Female; D006321:Heart / Q000033:anatomy & histology; D009124:Muscle Proteins / Q000378:metabolism*; D009218:Myosins / Q000378:metabolism; D009929:Organ Size; D051381:Rats; D012519:Sarcoplasmic Reticulum / Q000378:metabolism / Q000503:physiopathology*; D013550:Swimming
D009124:Muscle Proteins; D000205:Actomyosin; D000251:Adenosine Triphosphatases; D009218:Myosins; D002118:Calcium