The relationship of a decline in myofibrillar ATP-ase activity to the development of severe left ventricular hypertrophy in the rat.
Abdominal aortic coarctation in the rat led to a modest degree of cardiac hypertrophy associated with normal ATPase activity of myofibrills. The addition of aortic incompetence was accompanied by the development of severe hypertrophy (approx. 75 %). During the course of this latter increase in heart weight, the Ca++ ATPase of myofibrils progressively declined to a level 36% below controls. This occurred at a time when protein synthesis was stimulated as evidenced by increased incorporation of H3 lysine into myofibrils. Results are compatible with the hypothesis that the abnormal ATPase activity reflects the synthesis of an abnormal myosin molecule.
D000818:Animals; D000252:Calcium-Transporting ATPases / Q000378:metabolism*; D006332:Cardiomegaly / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D009124:Muscle Proteins / Q000096:biosynthesis*; D009210:Myofibrils / Q000201:enzymology / Q000378:metabolism; D009218:Myosins / Q000378:metabolism*; D051381:Rats
D009124:Muscle Proteins; D009218:Myosins; D000252:Calcium-Transporting ATPases