| First Author | Crozatier B | Year | 2002 |
| Journal | FASEB J | Volume | 16 |
| Issue | 7 | Pages | 653-60 |
| PubMed ID | 11978729 | Mgi Jnum | J:76204 |
| Mgi Id | MGI:2178859 | Doi | 10.1096/fj.01-0652com |
| Citation | Crozatier B, et al. (2002) Role of creatine kinase in cardiac excitation-contraction coupling: studies in creatine kinase-deficient mice. FASEB J 16(7):653-60 |
| abstractText | 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 beta-adrenergic stimulation. This shows the specific role of CK in excitation-contraction coupling in cardiac muscle that cannot be compensated for by other pathways. |
