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13 Distinct role of Ca2+–calmodulin-dependent protein kinase II in excitation–contraction coupling under certain conditions
  1. A Adameova1,
  2. T Ravingerova2
  1. 1Department of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University, Bratislava, Slovak Republik
  2. 2Institute for Heart Research and Centre of Excellence for Cardiovascular Research, Slovak Academy of Sciences, Bratislava, Slovak Republik


Ca2+-homeostatic proteins play an important role in Ca2+excitation–contraction coupling (ECC); however, the involvement of Ca2+calmodulin-dependent protein kinase II delta (CaMKII) in this process is less known. It has been suggested that CaMKII phosphorylates the key proteins for ECC including L-voltage Ca2+ channels (LTCC), which subsequently become longer in the open state. Such changes may initiate after depolarisations promoting arrhythmias and contractility disturbances.1 To test this hypothesis, KN-93 (0.5 μ/l), a CaMKII inhibitor, was administered into the perfusion solution before ischaemia and during the first 10 min of reperfusion. Incidence of ventricular fibrillation was decreased in the KN-treated rat hearts. Although the duration of arrhythmias did not differ between the groups, arrhythmia score was lower upon CaMKII inhibition. Likewise, the recovery of post-ischaemic contractile function was improved in the KN-treated hearts. On the other hand, no additive anti-arrhythmic effects of CaMKII inhibition were observed in the group treated with simvastatin (10 mg/kg, 7 days), which is known to suppress electrical instability.2 In the presence of CaMKII inhibitor in the simvastatin-treated group, the severity of arrhythmias was unchanged as compared with the group without treatment. However, CaMKII inhibitor reversed attenuation of post-ischaemic contractile dysfunction in simvastatin-treated rats. CaMKII and LTCC protein levels, which were lower in simvastatin-treated rats, were not influenced by KN treatment. In conclusion, CaMKII is involved in the mechanisms of ECC; however, it seems that under certain conditions, such as statins-mediated cardioprotection, it may have a distinct influence on excitation and contraction. Supported by VEGA 1/0620/10, 2/0173/08.

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