Rapid-cooling contracture in cardiac muscle is mediated by Ca2+ release from the sarcoplasmic reticulum through a mechanism independent of the ryanodine-sensitive pathway.
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Cooling-induced Ca2+ release from canine SR occurs independently of ryanodine receptors; leaves open its role in intact hearts or clinical hypothermia.
Rapid-cooling contracture in cardiac muscle preparations is thought to be caused by the release of Ca2+ from the sarcoplasmic reticulum (SR), but the mechanism of this release is unknown. Cooling of isolated canine cardiac SR from 37 to 4 degrees C resulted in the net release of enough Ca2+ to account for rapid-cooling contracture. The release of Ca2+ on cooling appeared to be a relaxation between different steady-state levels of Ca2+ uptake. Cooling release of Ca2+ was also observed in the presence of ryanodine or ruthenium red to block the ryanodine-sensitive Ca2+ efflux pathway. In the presence of ryanodine, the extent and initial rate of rapid-cooling release were increased due to increased steady-state uptake of Ca2+ by the SR. The first-order rate constant of rapid-cooling Ca2+ release was unchanged by ryanodine or ruthenium red, suggesting that the rapid-cooling release does not occur through the ryanodine-sensitive pathway. The alkalinization on cooling was not the major cause of the Ca2+ release, as comparable Ca2+ release was observed with cooling and no alkalinization. However, alkalinization without cooling produced a rapid net Ca2+ release, which was also observed in the presence of ryanodine.
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Feher et al. (1994) studied this question.
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