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Rate‐dependent changes of twitch force duration in rat cardiac trabeculae: a property of the contractile system
Author(s) -
Kassiri Z.,
Myers R.,
Kaprielian R.,
Banijamali H. S.,
Backx P. H.
Publication year - 2000
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2000.t01-3-00221.x
Subject(s) - chemistry , biophysics , isoprenaline , stimulation , contraction (grammar) , protein kinase a , calmodulin , medicine , kinetics , kinase , endocrinology , enzyme , biochemistry , biology , physics , quantum mechanics
1 We examined the mechanisms for rate‐dependent changes in twitch force duration by simultaneously measuring force and [Ca 2+ ] 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 [Ca 2+ ] i transients increased monotonically, whilst both force and [Ca 2+ ] i transient duration were abbreviated. 3 Changes in peak force or peak [Ca 2+ ] i transients were not responsible for the changes in force or [Ca 2+ ] i transient duration. 4 The changes in twitch force and [Ca 2+ ] 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 [Ca 2+ ] i transient kinetics, suggesting that protein kinase A (PKA), protein kinase PKG) and Ca 2+ ‐calmodulin‐dependent protein kinase II (CaM/kinase II) were not responsible for these kinetic changes. 6 Despite the changes in twitch force and [Ca 2+ ] 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 [Ca 2+ ] i transients do not depend on PKA or CaM/kinase II activity but might result from intrinsic features of the contractile and/or Ca 2+ ‐handling proteins.