Protein kinase A does not alter unloaded velocity of sarcomere shortening in skinned rat cardiac trabeculae.

Abstract

Whether beta-adrenergic stimulation affects the cross-bridge cycling rate independently of its effect on Ca2+ handling by the cardiac myocyte is still unknown. An increase in cross-bridge cycling rate may result in increased unloaded velocity of sarcomere shortening (V0). To test this hypothesis directly, skinned rat cardiac trabeculae were attached between a silicon strain gauge (approximately 3.5 kHz resonant frequency) and a fast displacement motor. V0 was measured by a modified "Edman slack test" during a single maximal activation using seven to eight sarcomere-length step releases (measured by laser diffraction) ranging between 0.12 and 0.20 micron (15.0 +/- 0.1 degrees C). beta-Adrenergic stimulation was mimicked by exposing the trabeculae to the catalytic subunit of protein kinase A (PKA). Treatment with PKA (3 micrograms/ml; 45 min) caused a significant (P < 0.01) increase (41 +/- 13%) in the Ca2+ concentration required for half-maximal steady-state tension development. Neither maximum tension nor V0 was affected by treatment with PKA, suggesting that beta-adrenergic stimulation does not affect the rate-limiting step of cross-bridge cycling during unloaded shortening in myocardium.