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The expression and regulation of Ca2+ signaling in embryonic cardiomyocytes has been shown to be different from those in adult heart cells, particularly the L-type Ca2+ channel current (I(CaL)) increases during development. However, little is known about the underlying reasons for this increase of I(CaL ) density and developmental changes in the process of I(CaL ) inactivation, a critical regulator of intracellular Ca2+ homeostasis. In the present work, we therefore studied functional differences of I(CaL) between embryonic and fetal cardiomyocytes and its interaction with intracellular Ca2+ homeostasis and Ca2+-induced Ca2+ release (CICR). Moreover, we examined the process of voltage- (VDI) and Ca2+-dependent inactivation (CDI) of I(CaL) during murine embryonic heart development.

cellular physiology and biochemistry

Functional Expression and Inactivation of L-type Ca&lt;sup&gt;2+&lt;/sup&gt; Currents During Murine Heart Development -Implications for Cardiac Ca&lt;sup&gt;2+&lt;/sup&gt; Homeostasis