Functional Expression and Inactivation of L-type Ca2+ Currents During Murine Heart Development -Implications for Cardiac Ca2+ Homeostasis | Zendy

Filomain Nguemo | Zendy; Bernd K. Fleischmann | Zendy; Heribert Schunkert | Zendy; Juergen Hescheler | Zendy; Michael Reppel | Zendy

Open Access

Functional Expression and Inactivation of L-type Ca<sup>2+</sup> Currents During Murine Heart Development -Implications for Cardiac Ca<sup>2+</sup> Homeostasis

Author(s) -

Filomain Nguemo,

Bernd K. Fleischmann,

Heribert Schunkert,

Juergen Hescheler,

Michael Reppel

Publication year - 2007

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000110441

Subject(s) - homeostasis , sarcolemma , embryonic heart , intracellular , chemistry , embryonic stem cell , myocyte , medicine , endocrinology , microbiology and biotechnology , biology , biochemistry , gene

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.

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