Key result
PKA treatment reduces calcium sensitivity in isolated human cardiac myofibrils without affecting crossbridge cycling kinetics.
Effect estimate: ΔpCa(50) = 0.2 ± 0.1
PKA treatment reduces calcium sensitivity in human cardiac myofibrils without directly altering crossbridge cycling kinetics.
PKA effects on isolated myofibrils should not change clinical practice; leaves open whether this mechanism alters intact cardiac function or disease outcomes.
We investigated the effect of PKA treatment (1 U/ml) on the mechanical properties of isolated human cardiac myofibrils. PKA treatment was associated with significant incorporation of radiolabeled phosphate into several sarcomeric proteins including troponin I and myosin binding protein C and was also associated with a right shift in the tension-pCa relation (ΔpCa(50) = 0.2 ± 0.1). PKA treatment also caused right shifts in the pCa dependence of the rate of tension development, tension redevelopment, and the linear and exponential phases of myofibril relaxation. However, there was no change in the same measures of crossbridge turnover when expressed as a function of tension. We conclude that the changes in crossbridge kinetics as a function of calcium concentration reflect a reduced tension due to a lower calcium sensitivity and that the relationship between crossbridge kinetics and tension was unchanged, indicating no direct effect of PKA treatment on crossbridge cycling.
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Walker et al. (2011) studied Isolated human cardiac myofibrils. PKA treatment was evaluated on Mechanical properties and crossbridge kinetics (ΔpCa(50) = 0.2 ± 0.1). PKA treatment of isolated human cardiac myofibrils reduced calcium sensitivity (ΔpCa(50) = 0.2 ± 0.1) without directly affecting crossbridge cycling kinetics.
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