BASIS FOR LATE RISE IN FURA 2-R SIGNAL REPORTING [CA2+](I) DURING RELAXATION IN INTACT RAT VENTRICULAR TRABECULAE

Intact rat ventricular trabeculae were injected with the salt form of fura 2, and the fura 2 ratio signal (R) was used to report intracellul ar Ca2+ concentration ([Ca2+](i)). The fixed end relaxation phase of a twitch is associated with a slowing of the decay of the R signal, or even a reversal, to form a distinct bump, indicating a transient rise in [Ca2+](i). The bump is most prominent at 30 degrees C, and motion a rtifact is not its cause. Increasing doses of 2,3-butanedione monoxime caused progressive attenuation of the twitch and bump. Increasing the bathing Ca2+ concentration potentiated the twitch and enhanced the bu mp. Imposed muscle shortening during relaxation caused a much quicker force decline, and this led to the appearance of a much more prominent associated bump. The amplitude of the bump depends on the amplitude o f twitch force and the rate of relaxation. These findings can be expla ined, as in skeletal muscle, by making cross-bridge attachment and Ca2 + binding to troponin C strongly cooperative; therefore, the bump duri ng fast relaxation is produced by a reversal of this cooperativity, le ading to rapid dissociation of Ca2+ from troponin C into the myoplasm.