PROTEIN-KINASE-A DOES NOT ALTER UNLOADED VELOCITY OF SARCOMERE SHORTENING IN SKINNED RAT CARDIAC TRABECULAE

Whether beta-adrenergic stimulation affects the cross-bridge cycling r ate independently of its effect on Ca2+ handling by the cardiac myocyt e is still unknown. An increase in cross-bridge cycling rate may resul t in increased unloaded velocity of sarcomere shortening (V-o). To tes t this hypothesis directly, skinned rat cardiac trabeculae were attach ed between a silicon strain gauge (similar to 3.5 kHz resonant frequen cy) and a fast displacement motor. V-o was measured by a modified ''Ed man slack test'' during a single maximal activation using seven to eig ht sarcomere-length step releases (measured by laser diffraction) rang ing between 0.12 and 0.20 mu m (15.0 +/- 0.1 degrees C). beta-Adrenerg ic stimulation was mimicked by exposing the trabeculae to the catalyti c subunit of protein kinase A (PKA). Treatment with PKA (3 mu g/ml; 45 min) caused a significant (P < 0.01) increase (41 +/- 13%) in the Ca2 + concentration required for half-maximal steady-state tension develop ment. Neither maximum tension nor V-o was affected by treatment with P KA, suggesting that beta-adrenergic stimulation does not affect the ra te-limiting step of cross-bridge cycling during unloaded shortening in myocardium.