| pubmed-article:8810775 | pubmed:abstractText | Contraction of cardiac muscle is regulated by intracellular Ca2+ concentration ([Ca2+]i) change. The Ca2+ increased by the action potential is removed by Ca2+ removal mechanisms (sarcoplasmic reticulum, Na-Ca exchanger and Ca pump of the surface membrane) and is also bound to troponin. However, under some specific conditions which induced an overload of Ca2+, oscillatory changes in [Ca2+]i, which are considered to be due to regenerative Ca2+ release from the sarcoplasmic reticulum, appear. In Ca2+ overload, a transient increase in [Ca2+]i is observed after the falling phase of the Ca2+ transient which is induced by electrical stimulation. In accordance with the transient increase in [Ca2+¿i, the membrane transiently depolarizes (delayed after-depolarization). This membrane depolarization is considered to be due to the inward currents through the Na-Ca exchanger and non-specific cation channels. If the depolarization is large enough to reach the threshold, the action potentials are triggered (triggered activity). Thus, an increase in [Ca2+]i is one of possible factors in triggering of arrhythmia. | lld:pubmed |
