RESUMO
Daily administration of d,l isoproterenol-HCl (5 mg/kg) in rats for periods of 14-21 days results in marked cardiac hypertrophy and a decrease in cardiac actomyosin ATPase activity. Actomyosin suspensions (ionic strength 0.08) from right and left ventricles showed average decreases in ATPase activity of 37.1% (p less than 0.005) and 35.7% (p less than 0.05), respectively, for animals treated with isoproterenol for 14 days. Isolated myofibrils from combined ventricular muscle of another group of animals that received the same isoproterenol treatment showed an average decrease in ATPase of 36.4% (p less than 0.0025). The later experiments also demonstrated that the decrease in ATPase activity was not Ca++ sensitive suggesting the lack of involvement of a change in the calcium regulatory factors (tropomyosin-troponin complex). In contrast to these findings, purified myosin from treated animals and actomyosin assayed under conditions which essentially reflect myosin ATPase activity uninfluenced by actin interaction (actomyosin in solution, ionic strength 0.6), did not demonstrate a change in ATPase from controls. It was concluded that the decrease in cardiac actomyosin ATPase in isoproterenol treated rats involved primarily a defect in actin or the interaction of actin with other components of the contractile protein complex.