Abstract
After sarcoplasmic reticulum (SR) Ca2+ depletion in intact ventricular
myocytes, electrical activity promotes SR Ca2+ reloading and recovery
of twitch amplitude. In ferret, recovery of twitch and caffeine-induced
contracture required fewer twitches than in rabbit or rat. In rat,
there was no difference in action potential duration at 90\% repolarization
(APD90) at steady state (SS) versus at the first post-depletion (PD)
twitch. The SS APD90 was similar in ferret and rabbit (but longer
than in rat). However, compared to SS, the PD APD90 was lengthened
in ferret, but shortened in rabbit. When rabbit myocytes were subjected
to AP-clamp patterns during SR Ca2+ reloading (ferret- or rabbit-type
APs), reloading was much faster using the ferret AP templates. We
conclude that the faster SR Ca2+ refilling in ferret is due to the
increased Ca2+ influx during the longer PD AP. The PD versus SS APD90
difference was suppressed by thapsigargin in ferret (indicating Ca2+
dependence). In rabbit, the PD AP shortening depended on the preceding
diastolic interval (rather than Ca2+), because rest produced the
same AP shortening, and SS APD90 increased as a function of frequency
(in contrast to ferret). Transient outward current (Ito) was larger
and recovered from inactivation much faster in ferret than in rabbit.
Moreover, slow Ito recovery (tau approximately 3 s) in rabbit was
a much larger fraction of Ito. Our data and a computational model
(including two Ito components) suggest that in rabbit the slowly
recovering Ito is responsible for short post-rest and PD APs, for
the unusual frequency dependence of APD90, and ultimately for the
slower post-depletion SR Ca2+ reloading.
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