Na+/Ca2+ Exchanger Knockout Mice: Plasticity of Cardiac Excitation-contraction Coupling.
From: Department of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Annals of the New York Academy of Sciences
- Publish Date: Mar 2007
- ISSN: 0077-8923
- Volume: 1099
- Issue:
- Pages: 270-5
- Medium: Print
- Language: English
- Citation (JAMA): Pott Christian, Henderson Scott A, Goldhaber Joshua I, et al. Na+/Ca2+ Exchanger Knockout Mice: Plasticity of Cardiac Excitation-contraction Coupling.. Ann. N. Y. Acad. Sci. Mar 2007;1099:270-5
Abstract
The Na+/Ca2+ exchanger (NCX) is the main Ca2+ extrusion mechanism of the cardiac myocyte. Nevertheless, cardiac-specific NCX knockout (KO) mice are viable to adulthood. We have identified two adaptations of excitation-contraction coupling (ECC) to the absence of NCX in these animals: (a) a reduction of the L-type Ca2+ current (I(Ca)) with an increase in ECC gain and (b) a shortening of the action potential (AP) to further limit Ca2+ influx. Both mechanisms contribute to Ca2+ homeostasis by reducing Ca2+ influx while maintaining contractility. These adaptations may comprise important feedback mechanisms by which cardiomyocytes may be able to limit Ca2+ influx in situations of compromised Ca2+ extrusion capacity.
Mesh Headings (Keywords): Action Potentials, Animals, Calcium Channels, L-Type, Mice, Mice, Knockout, Sodium-Calcium Exchanger
Check for Full Text / PubMed Unique Identifier (PMID): 17446467
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