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(The FASEB Journal. 2002;16:653-660.)
© 2002 FASEB

Role of creatine kinase in cardiac excitation-contraction coupling: studies in creatine kinase-deficient mice

BERTRAND CROZATIER*1, THIERRY BADOUAL*, ERNEST BOEHM{dagger},2, PIERRE-VLADIMIR ENNEZAT*, THIERRY GUENOUN*, JINBO SU*, VLADIMIR VEKSLER{dagger}, LUC HITTINGER* and RENÉE VENTURA-CLAPIER{dagger}

* Unité INSERM U 400, Créteil, France; and
{dagger} Unité INSERM U 446 Chatenay-Malabry, France

1Correspondence: Unité INSERM U 400, Faculté de Médecine, 8, rue du Général Sarrail 94000 Créteil, France. E-mail: crozatier{at}im3.inserm.fr

To understand the role of creatine kinase (CK) in cardiac excitation-contraction coupling, CK-deficient mice (CK-/-) were studied in vitro and in vivo. In skinned fibers, the kinetics of caffeine-induced release of Ca2+ was markedly slowed in CK-/- mice with a partial restoration when glycolytic substrates were added. These abnormalities were almost compensated for at the cellular level: the responses of Ca2+ transient and cell shortening to an increased pacing rate from 1 Hz to 4 Hz were normal with a normal post-rest potentiation of shortening. However, the post-rest potentiation of the Ca2+ transient was absent and the cellular contractile response to isoprenaline was decreased in CK-/- mice. In vivo, echocardiographically determined cardiac function was normal at rest but the response to isoprenaline was blunted in CK-/- mice. Previously described compensatory pathways (glycolytic pathway and closer sarcoplasmic reticulum-mitochondria interactions) allow a quasi-normal SR function in isolated cells and a normal basal in vivo ventricular function, but are not sufficient to cope with a large and rapid increase in energy demand produced by ß-adrenergic stimulation. This shows the specific role of CK in excitation-contraction coupling in cardiac muscle that cannot be compensated for by other pathways.—Crozatier, B., Badoual, T., Boehm, E., Ennezat, P.-V., Guenoun, T., Su, J., Veksler, V., Hittinger, L., Ventura-Clapier, R. Role of creatine kinase in cardiac excitation-contraction coupling: studies in creatine kinase-deficient mice.


Key Words: CK • ventricular function • cell shortening




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