Pott Christian, Goldhaber Joshua I, Philipson Kenneth D
Department of Physiology, David Geffen School of Medicine at UCLA, 675 Charles E. Young Dr. South, Los Angeles, CA 90095, USA.
Ann N Y Acad Sci. 2007 Mar;1099:310-4. doi: 10.1196/annals.1387.019.
Mice with homozygous overexpression of the Na+-Ca2+ exchanger (NCX) exhibit threefold levels of NCX expression and an increased Ca2+ extrusion rate. To investigate how Ca2+ homeostasis is maintained in this model, we have characterized Ca2+ influx under these conditions. We find that L-type Ca2+ currents (I(Ca)) inactivate slower due to a reduction of Ca2+-dependent inactivation. Additionally, NCX-overexpressing animals exhibit a prolongation of the action potential (AP). We conclude that transsarcolemmal Ca2+ fluxes in NCX-overexpressing myocytes are balanced by an increase in Ca2+ influx via (a) slowed inactivation of I(Ca) and (b) a prolongation of the AP to compensate for increased Ca2+ efflux.
钠钙交换体（NCX）纯合过表达的小鼠表现出三倍水平的NCX表达以及增加的钙离子外排速率。为了研究在该模型中钙离子稳态是如何维持的，我们对这些条件下的钙离子内流进行了表征。我们发现，由于钙依赖性失活的减少，L型钙电流（I(Ca)）失活较慢。此外，NCX过表达的动物表现出动作电位（AP）延长。我们得出结论，在NCX过表达的心肌细胞中，跨肌膜的钙离子通量通过以下方式得到平衡：（a）I(Ca)失活减慢导致钙离子内流增加，以及（b）AP延长以补偿增加的钙离子外流。
