ABSTRACT
The relationship between stimulation frequency and contraction was established for ventricular strips from rainbow trout heart at 5,15 and 25°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°C to a monophasic decline in force with increasing frequency at 25°C. Ryanodine reversed the negative force-frequency relationship at 25°C. Potentiation of twitch force after a 5 min rest period was increased from 121 ±4% at 15°C to 209±12% at 25°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°C. The ryanodine concentration causing a half-maximal reduction in rest potentiation of force was 51 nmol l−1 at 25°C and 483 nmol l−1 at 15°C. Rest potentiation was maximally reduced by 10μmoll−1 ryanodine to 50 and 79% of the value in the absence of ryanodine at 25 and 15°C, respectively. At 5°C, rest potentiation was similar to that at 15°C. At 5°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°C. Thus, in trout ventricle, force correlates with TPT at 5°C and seems to be regulated by a ryanodine-insensitive mechanism, while at 25°C force is correlated with the maximal rate of force development and the sarcoplasmic reticulum appears to contribute significantly to excitation-contraction coupling.
