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Rate-dependent changes of twitch force duration in rat cardiac trabeculae: a property of the contractile system

Z. Kassiri, R. Myers, R. Kaprielian, H. S. Banijamali and P. H. Backx

1. We examined the mechanisms for rate-dependent changes in twitch force duration by simultaneously measuring force and [Ca²⁺]_i in rat cardiac trabeculae.

2. Peak force decreased when the rate of stimulation was increased from 0·2 to 0·5 Hz, whilst it increased from 1 to 2 Hz. Over the same range of frequencies, peak [Ca²⁺]_i transients increased monotonically, whilst both force and [Ca²⁺]_i transient duration were abbreviated.

3. Changes in peak force or peak [Ca²⁺]_i transients were not responsible for the changes in force or [Ca²⁺]_i transient duration.

4. The changes in twitch force and [Ca²⁺]_i transient duration were completed roughly within one beat following an abrupt change in the rate of stimulation.

5. Rate-dependent changes resembled those observed with isoproterenol (isoprenaline) application. However, kinase inhibitors (i.e. K252-a, H-89, KN-62 and KN-93) had no effect on the rate-dependent changes of twitch force and [Ca²⁺]_i transient kinetics, suggesting that protein kinase A (PKA), protein kinase PKG) and Ca²⁺-calmodulin-dependent protein kinase II (CaM/kinase II) were not responsible for these kinetic changes.

6. Despite the changes in twitch force and [Ca²⁺]_i transient kinetics, the rate-limiting step for the rate-dependent force relaxation still resides at the level of the contractile proteins.

7. Our results suggest that rate-dependent changes in force and [Ca²⁺]_i transients do not depend on PKA or CaM/kinase II activity but might result from intrinsic features of the contractile and/or Ca²⁺-handling proteins.

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