The influence of temperature on ryanodine sensitivity and the force-frequency relationship in the myocardium of rainbow trout.

The relationship between stimulation frequency and contraction was established for ventricular strips from rainbow trout heart at 5, 15 and 25 degrees C. Compared to mammalian species, changes in temperature had little impact on force development in trout ventricle at physiologically relevant stimulation frequencies. However, the force-frequency relationship was changed from a biphasic response with a minimum around 0.2 Hz at 5 and 15 degrees C to a monophasic decline in force with increasing frequency at 25 degrees C. Ryanodine reversed the negative force-frequency relationship at 25 degrees C. Potentiation of twitch force after a 5 min rest period was increased from 121 +/- 4% at 15 degrees C to 209 +/- 12% at 25 degrees C. A similar augmentation was seen for the maximal rate of force development. Rest potentiation of both force and maximal rate of force development (dF/dT) was abolished by ryanodine at both 15 and 25 degrees C. The ryanodine concentration causing a half-maximal reduction in rest potentiation of force was 51 nmol l-1 at 25 degrees C and 483 nmol l-1 at 15 degrees C. Rest potentiation was maximally reduced by 10 mumol l-1 ryanodine to 50 and 79% of the value in the absence of ryanodine at 25 and 15 degrees C, respectively. At 5 degrees C, rest potentiation was similar to that at 15 degrees C. At 5 degrees C, there was no rest potentiation of dF/dT and ryanodine did not reduce rest potentiation of force. Instead, rest potentiation was correlated with a potentiation of time to peak tension (TPT) at 5 degrees C. Thus, in trout ventricle, force correlates with TPT at 5 degrees C and seems to be regulated by a ryanodine-insensitive mechanism, while at 25 degrees C force is correlated with the maximal rate of force development and the sarcoplasmic reticulum appears to contribute significantly to excitation-contraction coupling.