β-adrenergic effects on cardiac myofilaments and contraction in an integrated rabbit ventricular myocyte model

Journal of Molecular and Cellular Cardiology
Jorge A NegroniDonald M Bers

Abstract

A five-state model of myofilament contraction was integrated into a well-established rabbit ventricular myocyte model of ion channels, Ca(2+) transporters and kinase signaling to analyze the relative contribution of different phosphorylation targets to the overall mechanical response driven by β-adrenergic stimulation (β-AS). β-AS effect on sarcoplasmic reticulum Ca(2+) handling, Ca(2+), K(+) and Cl(-) currents, and Na(+)/K(+)-ATPase properties was included based on experimental data. The inotropic effect on the myofilaments was represented as reduced myofilament Ca(2+) sensitivity (XBCa) and titin stiffness, and increased cross-bridge (XB) cycling rate (XBcy). Assuming independent roles of XBCa and XBcy, the model reproduced experimental β-AS responses on action potentials and Ca(2+) transient amplitude and kinetics. It also replicated the behavior of force-Ca(2+), release-restretch, length-step, stiffness-frequency and force-velocity relationships, and increased force and shortening in isometric and isotonic twitch contractions. The β-AS effect was then switched off from individual targets to analyze their relative impact on contractility. Preventing β-AS effects on L-type Ca(2+) channels or phospholamban limited Ca(2+) trans...Continue Reading

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Nov 13, 2015·Wiley Interdisciplinary Reviews. Systems Biology and Medicine·Raimond L WinslowJoseph L Greenstein
Apr 9, 2017·American Journal of Physiology. Heart and Circulatory Physiology·E LascanoA Mattiazzi
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Feb 20, 2021·Mathematical Biosciences·Bogdan AmuzescuBeatrice Mihaela Radu
Nov 27, 2021·Physiological Reports·Mohamadamin ForouzandehmehrMichelangelo Paci

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