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Chronic pressure overload leads to hypertrophy, depressed mechanical function, and reduced myosin ATPase activity. However, it is not known whether the lowered myosin ATPase activity results from the hypertrophic process per se or whether the elevated afterload is required for the depressed myosin ATPase activity. Further, 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 that in pressure overload, allows the effects of pressure overload to be separated from the effects of hypertrophy and provides insight into the association between myosin ATPase and mechanical function. We produced large atrial septal defects (ASD) with a transvenous biopsy catheter in six 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 per second; ASD-1.02 + 0.26 muscle lengths per second), and normal (P > 0.05) myosin ATPase activity in three activating mediums (actin: C-0.20 ± 0.02, ASD «· 0.21 ± 0.03; Ca1+: C - 0.41 ± 0.03, ASD - 0.38 ± 0.02; K-EDTA: C - 1.67 ± 0.05, ASD - 1.69 ± 0.07 pmol Pi/min · ing). We concluded that pressure overload is required for depression of myosin ATPase activity. Our study supports the concept that depression of myosin ATPase is causally related to depressed mechanical function in chronic pressure overload. Circ Res 46: 81-87, 1979

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