Abstract
To determine whether catecholamines produce alterations in myocardialmyosin-actin cycling kinetics, we investigated the effects of isoproterenol upon mechanical characteristics of constantly activated heart muscle thought to reflect crossbridge behavior. In isolated rabbit right ventricular papillary muscles in barium contracture at 24°C, we found that 10 μm isoproterenol caused: (a) a 23% reduction of the 10 to 90% rise time of slow tension recovery in force transients induced by rapid, small amplitude stretches; and (b) a 23% increase in the frequency of sinusoidal length perturbation at which stiffness amplitude exhibited a minimum. Based upon previous mechanistic interpretations of force transients, and on an analysis developed here to relate crossbridge events to the frequency-dependence of stiffness, we argue that our observations provide evidence that isoproterenol induces an acceleration of crossbridge cycling rate. This raises the intriguing prospect that β-adrenergic stimulation regulates contraction, not only by well-known alterations in calcium metabolism, but also by intrinsic modulation of the force-generating machinery itself.
Original language | English (US) |
---|---|
Pages (from-to) | 415-426 |
Number of pages | 12 |
Journal | Journal of Molecular and Cellular Cardiology |
Volume | 20 |
Issue number | 5 |
DOIs | |
State | Published - May 1988 |
Externally published | Yes |
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cardiology and Cardiovascular Medicine
Keywords
- Barium contracture
- Catecholamines
- Crossbridge models
- Force transients
- Myocardial contractility
- Myosin-actin kinetics
- Segment stiffness