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Updated: Aug 11, 2026

Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling
Published on: August 1, 2016
Rest-dependence of twitch amplitude and sarcoplasmic reticulum calcium content in the developing rat myocardium
S A Ferraz1, J W Bassani, R A Bassani
1Centro de Engenharia Biomédica and Departmento de Engenharia Biomédica/Faculdade de Engenharia Elétrica e de Computação, Universidade Estadual de Campinas, 13083-970 Campinas, SP, Brazil.
Abstract:
Post-rest contractile response was studied in isolated ventricular muscle from rats aged 1 to 90 days. Amplitude of rapid cooling contractures (RCC) was taken as an index of the sarcoplasmic reticulum (SR) Ca2+ content. We observed that: (a) developed tension (per cross-section area) increased with age; (b) time to peak twitch force and relaxation half-time decreased from 87+/-6 to 56+/-2 ms and from 68+/-6 to 36+/-1 ms, respectively, from the neonatal period to adulthood; (c) post-rest twitch potentiation was observed at all ages, with greater relative potentiation in younger preparations, although relative potentiation of [Ca2+]i transient amplitude was similar in young and adult isolated ventricular myocytes; (d) rest did not significantly affect the amplitude of RCC in muscle or caffeine-evoked [Ca2+]i transients in myocytes at any studied age; (e) favoring Ca2+ efflux via Na+-Ca2+ exchange (NCX) during rest reversed twitch potentiation and caused a similar decrease in RCC amplitude ( approximately 40%) at all ages; (f) stimulation of Ca2+ influx via NCX during rest increased RCC amplitude ( approximately 40%) only in immature preparations. However, when this procedure was repeated after partial SR Ca2+ depletion, increase in RCC amplitude was not significantly age-dependent. We conclude that post-rest twitch potentiation is already present early after birth and does not require rest-dependent changes in SR Ca2+ content at any studied age. Our results suggest that NCX is close to equilibrium during rest in both adult and developing rat myocardium, and does not seem to mediate diastolic net Ca2+ fluxes which may affect the SR Ca2+ content.
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