%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 }