Me. Diaz et al., The role of intracellular Ca buffers in determining the shape of the systolic Ca transient in cardiac ventricular myocytes, PFLUG ARCH, 442(1), 2001, pp. 96-100
We have studied the kinetics of decay of cardiac Ca transients elicited by
either caffeine or electrical stimulation. The decay of the caffeine-evoked
increase of intracellular Ca concentration ([Ca2+](i)) could not be fit by
a single exponential. A two exponential fit showed an initial rapid compon
ent. The rate of decay of total Ca was calculated from measured free Ca and
the buffering properties of the cell. There was no initial rapid phase of
decay of total Ca. We conclude that the rapid phase of decay of free Ca is
due to a decrease of Ca buffering power at elevated [Ca2+](i). In contrast,
the decay of the Ca transient produced by voltage-clamp depolarization or
field stimulation was fit by a single exponential. We suggest that these ap
parently simple kinetics arise because a tendency to saturation at elevated
[Ca2+](i) of the sarcoplasmic reticulum Ca-ATPase offsets the decrease of
Ca buffering power. These data show the importance of Ca buffers as well as
transporters in determining the kinetics of changes of [Ca2+](i).