Can the Sodium-Calcium Exchanger Initiate or Suppress Calcium Sparks in Cardiac Myocytes?
作者： Daisuke Sato , Sanda Despa , Donald M. Bers
DOI: 10.1016/J.BPJ.2012.03.051
关键词:
摘要: Positive feedback of Calcium (Ca)-induced Ca release is the mechanism spark formation in cardiac myocytes. To initiate this process, a certain amount cleft space necessary. When membrane potential becomes higher during excitation-contraction coupling, can enter through both current (ICaL) and sodium-calcium exchanger (NCX) may activate ryanodine receptors to spark. On other hand, at resting (Vm ∼–80 mV), NCX removes from cell (forward mode). If released sarcoplasmic reticulum quickly removed via forward mode before Ca-induced starts, nonspark leak. This would also be influenced by the cleft/noncleft distribution NCX, which unknown. Using physiologically detailed mathematical model subcellular cycling, we analyze how strength alter formation. During most sparks are induced by ICaL with very few due current. At if localized cleft, spontaneous significantly reduced.
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