Key result
Homozygous overexpression of the Na+-Ca2+ exchanger in mice leads to balanced transsarcolemmal Ca2+ fluxes via slowed inactivation of L-type Ca2+ currents and prolonged action potentials.
Homozygous overexpression of NCX in mice leads to compensatory changes in Ca2+ influx, including slowed L-type Ca2+ current inactivation and prolonged action potentials.
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.
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Pott et al. (2007) studied Homozygous overexpression of the Na+-Ca2+ exchanger (NCX). Homozygous overexpression of the Na+-Ca2+ exchanger (NCX) was evaluated on Ca2+ influx and action potential characteristics. Homozygous overexpression of the Na+-Ca2+ exchanger in mice leads to balanced transsarcolemmal Ca2+ fluxes via slowed inactivation of L-type Ca2+ currents and prolonged action potentials.
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