Cardiac myocytes Ca$^2+$ and Na$^+$ regulation in normal
and failing hearts.
D. Bers, und S. Despa. J. Pharmacol. Sci., 100 (5):
315--322(2006)
Zusammenfassung
Ca$^2+$ is a central player in the excitation-contraction coupling
of cardiac myocytes, the process that enables the heart to contract
and relax. Mishandling of Ca$^2+$ is a central cause of both
contractile dysfunction and arrhythmias in pathophysiological conditions
such as heart failure (HF). Upon electrical excitation, Ca$^2+$
enters the myocytes via voltage-gated Ca$^2+$ channels and induces
further Ca$^2+$ release from the sarcoplasmic reticulum (SR).
This raises the free intracellular Ca$^2+$ concentration (Ca$^2+$(i)),
activating contraction. Relaxation is driven by Ca$^2+$(i)
decline, mainly due to re-uptake into the SR via SR Ca$^2+$-ATPase
and extrusion via the sarcolemmal Na$^+$/Ca$^2+$ exchange,
NCX. Intracellular Na$^+$ concentration (Na$^+$(i)) is
a main regulator of NCX, and thus Na$^+$(i) plays an important
role in controlling the cytosolic and SR Ca$^2+$. Na$^+$(i)
may have an even more important role in HF because NCX is generally
upregulated. There are several pathways for Na$^+$ entry into
the cells, whereas the Na$^+$/K$^+$ pump (NKA) is the main
Na$^+$ extrusion pathway and therefore is essential in maintaining
the transmembrane Na$^+$ gradient. Phospholemman is an important
regulator of NKA function (decreasing Na$^+$(i) affinity unless
it is phosphorylated). Here we discuss the interplay between Ca$^2+$
and Na$^+$ in myocytes from normal and failing hearts.
%0 Journal Article
%1 Bers_2006_315
%A Bers, Donald M
%A Despa, Sanda
%D 2006
%J J. Pharmacol. Sci.
%K Animals; Biological; Calciu; Cardiac; Congestive; Contraction; Exchanger; Failure, Heart Models, Myocardial Myocytes, Reticulum; Sarcoplasmic Sodium-Calcium Sodium; m
%N 5
%P 315--322
%T Cardiac myocytes Ca$^2+$ and Na$^+$ regulation in normal
and failing hearts.
%V 100
%X Ca$^2+$ is a central player in the excitation-contraction coupling
of cardiac myocytes, the process that enables the heart to contract
and relax. Mishandling of Ca$^2+$ is a central cause of both
contractile dysfunction and arrhythmias in pathophysiological conditions
such as heart failure (HF). Upon electrical excitation, Ca$^2+$
enters the myocytes via voltage-gated Ca$^2+$ channels and induces
further Ca$^2+$ release from the sarcoplasmic reticulum (SR).
This raises the free intracellular Ca$^2+$ concentration (Ca$^2+$(i)),
activating contraction. Relaxation is driven by Ca$^2+$(i)
decline, mainly due to re-uptake into the SR via SR Ca$^2+$-ATPase
and extrusion via the sarcolemmal Na$^+$/Ca$^2+$ exchange,
NCX. Intracellular Na$^+$ concentration (Na$^+$(i)) is
a main regulator of NCX, and thus Na$^+$(i) plays an important
role in controlling the cytosolic and SR Ca$^2+$. Na$^+$(i)
may have an even more important role in HF because NCX is generally
upregulated. There are several pathways for Na$^+$ entry into
the cells, whereas the Na$^+$/K$^+$ pump (NKA) is the main
Na$^+$ extrusion pathway and therefore is essential in maintaining
the transmembrane Na$^+$ gradient. Phospholemman is an important
regulator of NKA function (decreasing Na$^+$(i) affinity unless
it is phosphorylated). Here we discuss the interplay between Ca$^2+$
and Na$^+$ in myocytes from normal and failing hearts.
@article{Bers_2006_315,
abstract = {{C}a$^{2+}$ is a central player in the excitation-contraction coupling
of cardiac myocytes, the process that enables the heart to contract
and relax. Mishandling of {C}a$^{2+}$ is a central cause of both
contractile dysfunction and arrhythmias in pathophysiological conditions
such as heart failure (HF). Upon electrical excitation, {C}a$^{2+}$
enters the myocytes via voltage-gated {C}a$^{2+}$ channels and induces
further {C}a$^{2+}$ release from the sarcoplasmic reticulum (SR).
This raises the free intracellular {C}a$^{2+}$ concentration ([{C}a$^{2+}$](i)),
activating contraction. Relaxation is driven by [{C}a$^{2+}$](i)
decline, mainly due to re-uptake into the SR via SR {C}a$^{2+}$-ATPase
and extrusion via the sarcolemmal {N}a$^{+}$/{C}a$^{2+}$ exchange,
NCX. Intracellular {N}a$^{+}$ concentration ([{N}a$^{+}$](i)) is
a main regulator of NCX, and thus [{N}a$^{+}$](i) plays an important
role in controlling the cytosolic and SR [{C}a$^{2+}$]. [{N}a$^{+}$](i)
may have an even more important role in HF because NCX is generally
upregulated. There are several pathways for {N}a$^{+}$ entry into
the cells, whereas the {N}a$^{+}$/{K}$^{+}$ pump (NKA) is the main
{N}a$^{+}$ extrusion pathway and therefore is essential in maintaining
the transmembrane {N}a$^{+}$ gradient. Phospholemman is an important
regulator of NKA function (decreasing [{N}a$^{+}$](i) affinity unless
it is phosphorylated). Here we discuss the interplay between {C}a$^{2+}$
and {N}a$^{+}$ in myocytes from normal and failing hearts.},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Bers, Donald M and Despa, Sanda},
biburl = {https://www.bibsonomy.org/bibtex/2e6240f8c7509c7c721da8538e053ed3a/hake},
description = {The whole bibliography file I use.},
file = {Bers_2006_315.pdf:Bers_2006_315.pdf:PDF},
interhash = {01f8b8a8ce5d28a7b0fa84ccc887ff61},
intrahash = {e6240f8c7509c7c721da8538e053ed3a},
journal = {J. Pharmacol. Sci.},
keywords = {Animals; Biological; Calciu; Cardiac; Congestive; Contraction; Exchanger; Failure, Heart Models, Myocardial Myocytes, Reticulum; Sarcoplasmic Sodium-Calcium Sodium; m},
number = 5,
pages = {315--322},
pii = {JST.JSTAGE/jphs/CPJ06001X},
pmid = {16552170},
timestamp = {2009-06-03T11:21:03.000+0200},
title = {Cardiac myocytes {C}a$^{2+}$ and {N}a$^{+}$ regulation in normal
and failing hearts.},
volume = 100,
year = 2006
}