The Na$^+$/Ca$^2+$ exchanger (NCX) is the main Ca$^2+$
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 Ca$^2+$
current (I(Ca)) with an increase in ECC gain and (b) a shortening
of the action potential (AP) to further limit Ca$^2+$ influx.
Both mechanisms contribute to Ca$^2+$ homeostasis by reducing
Ca$^2+$ influx while maintaining contractility. These adaptations
may comprise important feedback mechanisms by which cardiomyocytes
may be able to limit Ca$^2+$ influx in situations of compromised
Ca$^2+$ extrusion capacity.
%0 Journal Article
%1 Pott_2007_270
%A Pott, Christian
%A Henderson, Scott A
%A Goldhaber, Joshua I
%A Philipson, Kenneth D
%D 2007
%J Ann. N. Y. Acad. Sci.
%K Action Animals; Calcium Channels, Exchanger, Knockout; L-Type, Mice, Mice; Potentials; Sodium-Calcium genetics/physiology physiology;
%P 270--275
%R 10.1196/annals.1387.015
%T Na$^+$/Ca$^2+$ exchanger knockout mice: plasticity of cardiac
excitation-contraction coupling.
%U http://dx.doi.org/10.1196/annals.1387.015
%V 1099
%X The Na$^+$/Ca$^2+$ exchanger (NCX) is the main Ca$^2+$
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 Ca$^2+$
current (I(Ca)) with an increase in ECC gain and (b) a shortening
of the action potential (AP) to further limit Ca$^2+$ influx.
Both mechanisms contribute to Ca$^2+$ homeostasis by reducing
Ca$^2+$ influx while maintaining contractility. These adaptations
may comprise important feedback mechanisms by which cardiomyocytes
may be able to limit Ca$^2+$ influx in situations of compromised
Ca$^2+$ extrusion capacity.
@article{Pott_2007_270,
abstract = {The {N}a$^{+}$/{C}a$^{2+}$ exchanger (NCX) is the main {C}a$^{2+}$
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 {C}a$^{2+}$
current (I(Ca)) with an increase in ECC gain and (b) a shortening
of the action potential (AP) to further limit {C}a$^{2+}$ influx.
Both mechanisms contribute to {C}a$^{2+}$ homeostasis by reducing
{C}a$^{2+}$ influx while maintaining contractility. These adaptations
may comprise important feedback mechanisms by which cardiomyocytes
may be able to limit {C}a$^{2+}$ influx in situations of compromised
{C}a$^{2+}$ extrusion capacity.},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Pott, Christian and Henderson, Scott A and Goldhaber, Joshua I and Philipson, Kenneth D},
biburl = {https://www.bibsonomy.org/bibtex/2047450f116529165280459696719f8e9/hake},
description = {The whole bibliography file I use.},
doi = {10.1196/annals.1387.015},
institution = {Department of Physiology, David Geffen School of Medicine at UCLA,
Los Angeles, CA 90095, USA.},
interhash = {ba0a7a36494fbf2504fc74dc32f09b39},
intrahash = {047450f116529165280459696719f8e9},
journal = {Ann. N. Y. Acad. Sci.},
keywords = {Action Animals; Calcium Channels, Exchanger, Knockout; L-Type, Mice, Mice; Potentials; Sodium-Calcium genetics/physiology physiology;},
month = Mar,
pages = {270--275},
pii = {1099/1/270},
pmid = {17446467},
timestamp = {2009-06-03T11:21:26.000+0200},
title = {{N}a$^{+}$/{C}a$^{2+}$ exchanger knockout mice: plasticity of cardiac
excitation-contraction coupling.},
url = {http://dx.doi.org/10.1196/annals.1387.015},
volume = 1099,
year = 2007
}