Effects of myocardial
hypertrophy caused by pressure overload on sarcolemmal Na+,K+-
ATPase and positive inotropic action of
strophanthidin were examined in cats. Partial
ligation of the main pulmonary artery for four weeks resulted in
right ventricular hypertrophy with no significant changes in left ventricular muscle.
Hypertrophy was associated with a reduction in the number of active Na+,K+-
ATPase units. Affinity of the remaining
enzyme for [3H]
ouabain was unchanged. No apparent right or left shift in dose-response curve for the positive inotropic effect of
strophanthidin was observed and toxic concentrations of
strophanthidin were unchanged; however, the degree of the positive inotropic effect produced by high concentrations of
strophanthidin was significantly smaller in hypertrophied muscle. Moreover, decreases in developed tension rather than
tachyarrhythmias was the predominant form of toxicity observed in hypertrophied muscle. These results indicate that myocardial
hypertrophy reduces the number of active Na+,K+-
ATPase units per milligram
protein, decreases maximal positive inotropic effect of
strophanthidin, and alters the prevailing form of
strophanthidin toxicity.