Thyroxine-induced cardiomegaly: assessment of nucleic acid, protein content and myosin ATPase of rat heart.
1 mg/kg L-thyroxine was administered to rats for 14 days to evaluate the potential of the hyperthyroid state to induce heart hypertrophy and its effect on myosin adenosine-triphosphatase (ATPase) activity. Evidence of hyperthyroidism such as weight loss, elevation of rectal temperature, increased heart rate and oxygen consumption, was observed in all treated rats. Cardiac enlargement was determined by comparison of wet and dry ventricle weights, myocardial RNA, DNA and protein content. Wet and dry ventricle weights and the level of cardiac RNA and protein were augmented by thyroxine treatment. ATPase activity of cardiac myosin was stimulated as the Ca2+ concentration in the incubation medium increased. No difference was found in Ca2+-activation, salt sensitivity or ATPase activity of unreacted and sulphydrylmodified cardiac myosins from euthyroid or hyperthyroid groups. The results showed that in hyperthyroid rats, in contrast to some other species, the biochemical mechanism responsible for the enhancement of cardiac contractility is not an increased myosin ATPase.
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000818:Animals; D001835:Body Weight; D006332:Cardiomegaly / Q000139:chemically induced* / Q000378:metabolism; D002729:Chloromercuribenzoates / Q000494:pharmacology; D004247:DNA / Q000378:metabolism*; D008297:Male; D009124:Muscle Proteins / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D009218:Myosins / Q000378:metabolism; D009929:Organ Size; D012313:RNA / Q000378:metabolism*; D051381:Rats; D013974:Thyroxine / Q000009:adverse effects*
D002729:Chloromercuribenzoates; D009124:Muscle Proteins; D012313:RNA; D004247:DNA; D000251:Adenosine Triphosphatases; D009218:Myosins; D013974:Thyroxine