Key result
Beta-adrenergic stimulation with isoproterenol or PKA increased the unloaded shortening velocity of skinned single rat ventricular myocytes by 38% and 41%, respectively.
Why the study?
Does beta-adrenergic stimulation increase unloaded shortening velocity in rat ventricular myocytes?
Population
Single rat ventricular myocytes (enzymatically isolated, skinned)
Comparison
Isoproterenol or cAMP-dependent protein kinase vs Ringer's solution without ISO/PKA (control cells)
Design
Preclinical
Authors
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No immediate clinical implications; leaves open translation of rat myofilament velocity effects to human contractility.
Does beta-adrenergic stimulation increase unloaded shortening velocity in rat ventricular myocytes?
Beta-adrenergic stimulation increases the rate of crossbridge release from actin in rat ventricular myocytes, likely via phosphorylation of troponin I and/or C protein by PKA.
Strang et al. (1994) studied this question. Isoproterenol (ISO) and cAMP-dependent protein kinase (PKA) vs. Control (Ringer's solution without ISO) was evaluated on Unloaded shortening velocity (Vo). Beta-adrenergic stimulation with isoproterenol or PKA increased the unloaded shortening velocity of skinned single rat ventricular myocytes by 38% and 41%, respectively.
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