Sarcolemmal and Sarcoplasmic Reticular ATPase Activities in the Falling Canine Heart
The specific activity of both the sarcoleminal Na+-K+-activated and the sarcoplasmic reticular ATPase systems was studied in dogs with right ventricular hypertrophy and congestive heart failure induced by progressive pulmonary artery stenosis. In these enzyme preparations, mitochondrial or cross contamination of either of the cellular fractions studied did not appear to be a factor. In the sarcoplasmic reticular fraction, ouabain was without effect and succinic dehydrogenase assay showed less that 10% of the activity observed in pure mitochondrial preparations. In the sarcolemmal fraction, sodium azide did not significantly inhibit the ATPase activity, but ouabain inhibited 91% of it. The activity of the sarcolemmal ATPase system of the faihng heart did not differ from that of the control; however, the activity of failing heart sarcolemmal preparations was found to be only 61% inhibited by 10-4M ouabain, and the activity of control preparations was 91% inhibited. The sarcoplasinic reticular ATPase activity from right ventricles of dogs with congestive heart failure was significantly less (P<0.001) than the respective control activity (average 15.9 compared to 28.1 µmole hr-1 mg-1), whereas the activity from left ventricles of failing hearts did not differ significantly from the respective control value. These findings suggest that a possible explanation for the diminished contractility of the chronically failing heart lies within the subcellular enzymatic ion-regulating systems.
- Na+-K+ ATPase
- congestive heart failure
- pulmonary artery stenosis
- myocardial contractility
- right ventricular hypertrophy
- Received November 30, 1970.
- Accepted April 19, 1971.
- © 1971 American Heart Association, Inc.