In rat ventricular myocytes, local caffeine application initiates propagating calcium waves that depend on sarcoplasmic reticulum calcium content, providing insights into cellular calcium dynamics.
No immediate clinical implications for arrhythmia therapy; extends in vitro models of SR Ca2+–dependent wave propagation.
Caffeine was applied locally to one region of a resting cell via an extracellular pipette while simultaneously imaging the concentrations of intracellular calcium ([Ca2+]i) and intracellular caffeine ([caffeine]i). 2. Local application of caffeine produced a rise of [caffeine]i which was confined to the region of the cell near the pipette. There was also a local increase of [Ca2+]i which then, in most resting cells, propagated along the cell as a linear Ca2+ wave. The initial magnitude of the rise of [Ca2+]i was greater than that of the electrically stimulated Ca2+ transient. 3. As the wave of increase of [Ca2+]i propagated along the cell it decreased in both amplitude and velocity in cells that had not been treated to elevate the cellular Ca2+ load. 4. In some cells the caffeine response did not propagate significantly. In these cases an increase of the cellular Ca2+ load enabled caffeine-induced Ca2+ wave propagation along the entire cell length without significant decay in amplitude and velocity. 5. Previous work has shown that an electrically evoked local systolic Ca2+ transient does not propagate. The fact that the caffeine-evoked response does propagate and the correlation between decay of amplitude and velocity suggest that the transient has to be a certain size before it can propagate. It is suggested that one of the factors which favour propagation of waves under conditions of elevated sarcoplasmic reticulum Ca2+ content is the increased release of Ca2+.
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Trafford et al. (1995) studied this question.
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