Myosin adenosine triphosphatase activity in the volume-overloaded hypertrophied feline right ventricle.

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Abstract
Chronic pressure overload leads to hypertrophy, depressed mechanical function and reduced myosin ATPase activity. Whether the lowered myosin ATPase activity results from the hypertrophic process per se or whether the elevated after load is required for the depressed myosin ATPase activity is not known. A causal relationship between lowered myosin ATPase and weakened mechanical function in pressure overload has not been established. Chronic volume overload on the myocardium, leading to hypertrophy equivalent to thbt in pressure overload, allows the effects of pressure overload to be separated from the effects of hypertrophy and explains the association between myosin ATPase and mechanical function. Large atrial septal defects (ASD) were produced with a transvenous biopsy catheter in 6 adult cats. This resulted in 63% right ventricular hypertrophy, normal (P > 0.05) papillary muscle mechanical function (velocity at 0.5 g/mm2 load: control = 1.01 .+-. 0.05 muscle lengths/s; ASD = 1.02 .+-. 0.26 muscle lengths/s), and normal (P > 0.05) myosin ATPase activity in 3 activating mediums (actin: C [correlation coefficient] = 0.20 .+-. 0.02, ASD = 0.21 .+-. 0.03; Ca2+: C = 0.41 .+-. 0.03, ASD = 0.38 .+-. 0.02; K-EDTA: C = 1.67 .+-. 0.05, ADS = 1.69 .+-. 0.07 .mu.mol Pi/min .cntdot. mg). Pressure overload is apparently required for depression of myosin ATPase activity. The concept that depression of myosin ATPase is causally related to depressed mechanical function in chronic pressure overload is supported.