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Sarcomere length dependence of power output is increased after PKA treatment in rat cardiac myocytes

Department of Physiology, University of Missouri School of Medicine, Columbia, Missouri

Submitted 6 August 2008 ; accepted in final form 23 February 2009

The Frank-Starling relationship of the heart yields increased stroke volume with greater end-diastolic volume, and this relationship is steeper after β-adrenergic stimulation. The underlying basis for the Frank-Starling mechanism involves length-dependent changes in both Ca²⁺ sensitivity of myofibrillar force and power output. In this study, we tested the hypothesis that PKA-induced phosphorylation of myofibrillar proteins would increase the length dependence of myofibrillar power output, which would provide a myofibrillar basis to, in part, explain the steeper Frank-Starling relations after β-adrenergic stimulation. For these experiments, adult rat left ventricles were mechanically disrupted, permeabilized cardiac myocyte preparations were attached between a force transducer and position motor, and the length dependence of loaded shortening and power output were measured before and after treatment with PKA. PKA increased the phosphorylation of myosin binding protein C and cardiac troponin I, as assessed by autoradiography. In terms of myocyte mechanics, PKA decreased the Ca²⁺ sensitivity of force and increased loaded shortening and power output at all relative loads when the myocyte preparations were at long sarcomere length (2.30 µm). PKA had less of an effect on loaded shortening and power output at short sarcomere length (2.0 µm). These changes resulted in a greater length dependence of myocyte power output after PKA treatment; peak normalized power output increased 20% with length before PKA and 40% after PKA. These results suggest that PKA-induced phosphorylation of myofibrillar proteins explains, in part, the steeper ventricular function curves (i.e., Frank-Starling relationship) after β-adrenergic stimulation of the left ventricle.

Frank-Starling; protein kinase A; myosin binding protein C; cardiac troponin I