Mechanical restitution and post-rest potentiation in isolated rat atria were studied in order to understand the intracellular Ca 2+ handling during stimulation and interbeat interval. Various agents known to affect transmembrane Ca 2+ inward current or Ca 2+ accumulation of the sarcoplasmic reticulum were examined. The tissues were stimulated at 1 Hz and ectopic stimuli of different preceding intervals were driven by a programmable stimulator. The relationship between the force produced by the ectopic contraction and the duration of the preceding interval was plotted to construct mechanical restitution curves. Mechanical restitution curve was well fitted to two exponential processes, i.e., an early rapid phase followed by a slowly rising phase. It is suggested that the time constant in early phase (τ 1 ) of mechanical restitution curve is dependent on the reactivation of transmembrane Ca 2+ inward currents as well as the translocation of Ca 2+ within the sarcoplasmic reticulum. However, the time constant in late phase (τ 2 ) involves the rate of Ca 2+ influx or efflux possibly via the Na + /Ca 2+ exchange mechanism. The present studies suggest that in rat myocardium, verapamil enhances the buffering capacity of the sarcoplasmic reticulum inside the cell, while isoproterenol appears to short circuit the buffering barrier of the sarcoplasmic reticulum and enhance the flow of Ca 2+ into the cytosol. Ryanodine, which accelerates the Ca 2+ release from the sarcoplasmic reticulum, is believed to attenuate its buffering capacity. The present analytical methods to which the mechanical restitution and the post-rest potentiation are combined would represent a good model for the study of beat-to-beat intracellular Ca2+ handling in cardiac muscle.
|Number of pages||7|
|Journal||Chinese Journal of Physiology|
|Publication status||Published - 1996 Jan 1|
All Science Journal Classification (ASJC) codes
- Physiology (medical)