Role of Ca(2+) in the rapid cooling-induced Ca(2+) release from sarcoplasmic reticulum in ferret cardiac muscles.

Rapid lowering of the solution temperature (rapid cooling, RC) from 24 to 3°C within 3 s releases considerable amounts of Ca(2+) from the sarcoplasmic reticulum (SR) in mammalian cardiac muscles. In this study, we investigated the intracellular mechanism of RC-induced Ca(2+) release, especially the role of Ca(2+), in ferret ventricular muscle. Saponin-treated skinned trabeculae were placed in a glass capillary, and the amount of Ca(2+) released from the SR by RC and caffeine (50 mM) was measured with fluo-3. It was estimated that in the presence of ATP about 45% of the Ca(2+) content in the SR was released by RC. The amount of SR Ca(2+) released by RC was unchanged by the replacement of ATP by AMP-PCP (a non-hydrolysable ATP analogue and agonist for the ryanodine receptor but not for the Ca(2+) pump of SR), suggesting that the suppression of the Ca(2+) pump of SR at low temperature might not be a major mechanism in RC-induced Ca(2+) release. The free Ca(2+) concentration of the solution used for triggering RC-induced Ca(2+) release was estimated to be only about 20 nM with fluo-3 or aequorin. When this solution was applied to the preparation at 3°C, only a small amount of Ca(2+) was released from SR presumably by the Ca(2+)-induced Ca(2+) release (CICR) mechanism. Thus, in mammalian cardiac muscles, RC releases a part of the (<50%) stored Ca(2+) contained in the SR, and the mechanism of RC-induced Ca(2+) release may differ from that of CICR, which is thought to play a role in frog skeletal muscle fibres that express ryanodine receptors of different types.