Cardiac excitation–contraction coupling

Of the ions involved in the intricate workings of the heart, calcium is considered perhaps the most important. It is crucial to the very process that enables the chambers of the heart to contract and relax, a process called excitation–contraction coupling. It is important to understand in quantitative detail exactly how calcium is moved around the various organelles of the myocyte in order to bring about excitation–contraction coupling if we are to understand the basic physiology of heart function. Furthermore, spatial microdomains within the cell are important in localizing the molecular players that orchestrate cardiac function.

[1]  F. Plum Handbook of Physiology. , 1960 .

[2]  S. Winegrad Calcium release from cardiac sarcoplasmic reticulum. , 1982, Annual review of physiology.

[3]  A. Fabiato,et al.  Rapid ionic modifications during the aequorin-detected calcium transient in a skinned canine cardiac Purkinje cell , 1985, The Journal of general physiology.

[4]  G. Vassort,et al.  Inositol phosphate production following α1‐adrenergic, muscarinic or electrical stimulation in isolated rat heart , 1986, FEBS letters.

[5]  J. Putney Phosphoinositides and receptor mechanisms , 1986 .

[6]  N. Leblanc,et al.  Sodium current-induced release of calcium from cardiac sarcoplasmic reticulum. , 1990, Science.

[7]  C. Sumners,et al.  Regulation of angiotensin II binding sites in neuronal cultures by protein kinase C. , 1990, The American journal of physiology.

[8]  Donald M. Bers,et al.  Excitation-Contraction Coupling and Cardiac Contractile Force , 1991, Developments in Cardiovascular Medicine.

[9]  M. Stern,et al.  Theory of excitation-contraction coupling in cardiac muscle. , 1992, Biophysical journal.

[10]  M. Morad,et al.  Gating of the cardiac Ca2+ release channel: the role of Na+ current and Na(+)-Ca2+ exchange. , 1992, Science.

[11]  L. Brunton,et al.  Excitation-contraction coupling and cardiac contractile force , 1992 .

[12]  D. Bers,et al.  Sarcoplasmic reticulum Ca2+ uptake and thapsigargin sensitivity in permeabilized rabbit and rat ventricular myocytes. , 1993, Circulation research.

[13]  S. Györke,et al.  Ryanodine receptor adaptation: control mechanism of Ca(2+)-induced Ca2+ release in heart. , 1993, Science.

[14]  W. Giles,et al.  Role of sodium‐calcium exchange in activation of contraction in rat ventricle. , 1993, The Journal of physiology.

[15]  W. Lederer,et al.  Calcium sparks: elementary events underlying excitation-contraction coupling in heart muscle. , 1993, Science.

[16]  P. Lipp,et al.  Sodium current‐induced calcium signals in isolated guinea‐pig ventricular myocytes. , 1994, The Journal of physiology.

[17]  O. Kohmoto,et al.  Depolarization-induced Ca entry via Na-Ca exchange triggers SR release in guinea pig cardiac myocytes. , 1994, The American journal of physiology.

[18]  R A Bassani,et al.  Relaxation in rabbit and rat cardiac cells: species‐dependent differences in cellular mechanisms. , 1994, The Journal of physiology.

[19]  N. Leblanc,et al.  Release of calcium from guinea pig cardiac sarcoplasmic reticulum induced by sodium-calcium exchange. , 1994, Cardiovascular research.

[20]  G. Isenberg,et al.  Ca2+ activation and Ca2+ inactivation of canine reconstituted cardiac sarcoplasmic reticulum Ca(2+)‐release channels. , 1995, The Journal of physiology.

[21]  R. Sitsapesan,et al.  New insights into the gating mechanisms of cardiac ryanodine receptors revealed by rapid changes in ligand concentration. , 1995, Circulation research.

[22]  A. Pappano,et al.  Na+ current and Ca2+ release from the sarcoplasmic reticulum during action potentials in guinea‐pig ventricular myocytes. , 1995, The Journal of physiology.

[23]  S. Lemaire,et al.  Tetrodotoxin-sensitive Ca2+ and Ba2+ currents in human atrial cells. , 1995, Receptors & channels.

[24]  C W Balke,et al.  Local calcium transients triggered by single L-type calcium channel currents in cardiac cells. , 1995, Science.

[25]  W Yuan,et al.  Fractional SR Ca release is regulated by trigger Ca and SR Ca content in cardiac myocytes. , 1995, The American journal of physiology.

[26]  M. Diaz,et al.  Comparison of subsarcolemmal and bulk calcium concentration during spontaneous calcium release in rat ventricular myocytes. , 1995, The Journal of physiology.

[27]  G. Ellis‐Davies,et al.  Rapid adaptation of cardiac ryanodine receptors: modulation by Mg2+ and phosphorylation. , 1995, Science.

[28]  W. Lederer,et al.  The control of calcium release in heart muscle. , 1995, Science.

[29]  K. Sipido,et al.  Inhibition and rapid recovery of Ca2+ current during Ca2+ release from sarcoplasmic reticulum in guinea pig ventricular myocytes. , 1995, Circulation research.

[30]  D. Bers,et al.  Steady-state twitch Ca2+ fluxes and cytosolic Ca2+ buffering in rabbit ventricular myocytes. , 1996, The American journal of physiology.

[31]  Cardiac alpha(1)-adrenoceptors that regulate contractile function: subtypes and subcellular signal transduction mechanisms. , 1996, Neurochemical research.

[32]  G. Langer,et al.  Calcium concentration and movement in the diadic cleft space of the cardiac ventricular cell. , 1996, Biophysical journal.

[33]  Yvonne M. Kobayashi,et al.  Complex Formation between Junctin, Triadin, Calsequestrin, and the Ryanodine Receptor , 1997, The Journal of Biological Chemistry.

[34]  R. Robinson,et al.  beta 1-and beta 2-adrenergic receptors exhibit differing susceptibility to muscarinic accentuated antagonism. , 1997, The American journal of physiology.

[35]  C. Korbmacher,et al.  cAMP stimulates CFTR-like Cl- channels and inhibits amiloride-sensitive Na+ channels in mouse CCD cells. , 1997, The American journal of physiology.

[36]  D. Bers,et al.  Effects of [Ca2+]i, SR Ca2+ load, and rest on Ca2+ spark frequency in ventricular myocytes. , 1997, The American journal of physiology.

[37]  D. Bers,et al.  Intracellular Ca2+ increases the mitochondrial NADH concentration during elevated work in intact cardiac muscle. , 1997, Circulation research.

[38]  H. Schulman,et al.  The Nuclear δB Isoform of Ca2+/Calmodulin-dependent Protein Kinase II Regulates Atrial Natriuretic Factor Gene Expression in Ventricular Myocytes* , 1997, The Journal of Biological Chemistry.

[39]  M. Fill,et al.  Identification and Functional Reconstitution of the Type 2 Inositol 1,4,5-Trisphosphate Receptor from Ventricular Cardiac Myocytes* , 1997, The Journal of Biological Chemistry.

[40]  M. Diaz,et al.  Enhanced calcium current and decreased calcium efflux restore sarcoplasmic reticulum Ca content following depletion , 1997 .

[41]  L. Goldman,et al.  Tetrodotoxin‐blockable calcium currents in rat ventricular myocytes; a third type of cardiac cell sodium current , 1997, The Journal of physiology.

[42]  F Van de Werf,et al.  Low efficiency of Ca2+ entry through the Na(+)-Ca2+ exchanger as trigger for Ca2+ release from the sarcoplasmic reticulum. A comparison between L-type Ca2+ current and reverse-mode Na(+)-Ca2+ exchange. , 1997, Circulation research.

[43]  C. January,et al.  Both T- and L-type Ca2+ channels can contribute to excitation-contraction coupling in cardiac Purkinje cells. , 1998, Biophysical journal.

[44]  E. Lakatta,et al.  Termination of Ca2+ release by a local inactivation of ryanodine receptors in cardiac myocytes. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[45]  F. Werf,et al.  T‐type Ca2+ current as a trigger for Ca2+ release from the sarcoplasmic reticulum in guinea‐pig ventricular myocytes , 1998, The Journal of physiology.

[46]  D. Bers,et al.  Cardiac myocyte calcium transport in phospholamban knockout mouse: relaxation and endogenous CaMKII effects. , 1998, American journal of physiology. Heart and circulatory physiology.

[47]  G. Hasenfuss,et al.  Alterations of calcium-regulatory proteins in heart failure. , 1998, Cardiovascular research.

[48]  Sandor Györke,et al.  Termination of Ca2+ release during Ca2+ sparks in rat ventricular myocytes , 1998, The Journal of physiology.

[49]  S. Litwin,et al.  Na-Ca exchange and the trigger for sarcoplasmic reticulum Ca release: studies in adult rabbit ventricular myocytes. , 1998, Biophysical journal.

[50]  W. Lederer,et al.  Ca2+ flux through promiscuous cardiac Na+ channels: slip-mode conductance. , 1998, Science.

[51]  G. Fishman,et al.  Sorcin Associates with the Pore-forming Subunit of Voltage-dependent L-type Ca2+ Channels* , 1998, The Journal of Biological Chemistry.

[52]  E. Lakatta,et al.  Opposing effects of α1-adrenergic receptor subtypes on Ca2+ and pH homeostasis in rat cardiac myocytes. , 1998, American journal of physiology. Heart and circulatory physiology.

[53]  R. Solaro,et al.  Troponin and tropomyosin: proteins that switch on and tune in the activity of cardiac myofilaments. , 1998, Circulation research.

[54]  E. Marbán,et al.  Whether "Slip-Mode Conductance" Occurs , 1999, Science.

[55]  E. Lakatta,et al.  beta2-adrenergic cAMP signaling is uncoupled from phosphorylation of cytoplasmic proteins in canine heart. , 1999, Circulation.

[56]  S. Steinberg,et al.  Activated protein kinase C isoforms target to cardiomyocyte caveolae : stimulation of local protein phosphorylation. , 1999, Circulation research.

[57]  J L Puglisi,et al.  Ca(2+) influx through Ca(2+) channels in rabbit ventricular myocytes during action potential clamp: influence of temperature. , 1999, Circulation research.

[58]  C. Starmer,et al.  beta-Adrenergic action on wild-type and KPQ mutant human cardiac Na+ channels: shift in gating but no change in Ca2+:Na+ selectivity. , 1999, Cardiovascular research.

[59]  D. T. Yue,et al.  Calmodulin Is the Ca2+ Sensor for Ca2+-Dependent Inactivation of L-Type Calcium Channels , 1999, Neuron.

[60]  K. Deisseroth,et al.  Calmodulin supports both inactivation and facilitation of L-type calcium channels , 1999, Nature.

[61]  F. Protasi,et al.  Shape, size, and distribution of Ca(2+) release units and couplons in skeletal and cardiac muscles. , 1999, Biophysical journal.

[62]  P R Ershler,et al.  Properties of Ca2+ sparks evoked by action potentials in mouse ventricular myocytes , 1999, The Journal of physiology.

[63]  C W Balke,et al.  Ca(2+) release mechanisms, Ca(2+) sparks, and local control of excitation-contraction coupling in normal heart muscle. , 1999, Circulation research.

[64]  A. Zahradníková,et al.  Rapid Activation of the Cardiac Ryanodine Receptor by Submillisecond Calcium Stimuli , 1999, The Journal of General Physiology.

[65]  S. Lehnart,et al.  Relationship between Na+-Ca2+-exchanger protein levels and diastolic function of failing human myocardium. , 1999, Circulation.

[66]  S. Houser,et al.  The sarcoplasmic reticulum and the Na+/Ca2+ exchanger both contribute to the Ca2+ transient of failing human ventricular myocytes. , 1999, Circulation research.

[67]  M. Diaz,et al.  Integrative Analysis of Calcium Cycling in Cardiac Muscle , 2000, Circulation research.

[68]  D. Bers,et al.  Phosphorylation of phospholamban and troponin I in beta-adrenergic-induced acceleration of cardiac relaxation. , 2000, American journal of physiology. Heart and circulatory physiology.

[69]  D. Bers,et al.  Potentiation of fractional sarcoplasmic reticulum calcium release by total and free intra-sarcoplasmic reticulum calcium concentration. , 2000, Biophysical journal.

[70]  S. Matsuoka,et al.  Stoichiometry of Na+‐Ca2+ exchange in inside‐out patches excised from guinea‐pig ventricular myocytes , 2000, The Journal of physiology.

[71]  T. Wiesner,et al.  Inhibition of Ca2+ Sparks by Ruthenium Red in Permeabilized Rat Ventricular Myocytes , 2000 .

[72]  E. Kranias,et al.  Phospholamban and cardiac contractile function. , 2000, Journal of molecular and cellular cardiology.

[73]  S. Houser,et al.  Voltage‐dependent Ca2+ release from the SR of feline ventricular myocytes is explained by Ca2+‐induced Ca2+ release , 2000, The Journal of physiology.

[74]  M. Berridge,et al.  Functional InsP3 receptors that may modulate excitation–contraction coupling in the heart , 2000, Current Biology.

[75]  P. Dan,et al.  Distribution of proteins implicated in excitation-contraction coupling in rat ventricular myocytes. , 2000, Biophysical journal.

[76]  T. Wiesner,et al.  Inhibition of Ca(2+) sparks by ruthenium red in permeabilized rat ventricular myocytes. , 2000, Biophysical journal.

[77]  G. Strasburg,et al.  Differential Ca(2+) sensitivity of skeletal and cardiac muscle ryanodine receptors in the presence of calmodulin. , 2000, American journal of physiology. Cell physiology.

[78]  D. Burkhoff,et al.  PKA Phosphorylation Dissociates FKBP12.6 from the Calcium Release Channel (Ryanodine Receptor) Defective Regulation in Failing Hearts , 2000, Cell.

[79]  E Niggli,et al.  Paradoxical block of the Na+‐Ca2+ exchanger by extracellular protons in guinea‐pig ventricular myocytes , 2000, The Journal of physiology.

[80]  M. Egger,et al.  L‐type Ca2+ current as the predominant pathway of Ca2+ entry during INa activation in β‐stimulated cardiac myocytes , 2000, The Journal of physiology.

[81]  S. Emani,et al.  Cardiac Gene Delivery With Cardiopulmonary Bypass , 2001, Circulation.

[82]  Erratum: A β2 adrenergic receptor signaling complex assembled with the Ca2+ channel Cav1.2 (Science (July 6) (98)) , 2001 .

[83]  S. Sollott,et al.  Glucagon-Like Peptide-1 Increases cAMP but Fails to Augment Contraction in Adult Rat Cardiac Myocytes , 2001, Circulation research.

[84]  Li Li,et al.  Arrhythmogenesis and Contractile Dysfunction in Heart Failure: Roles of Sodium-Calcium Exchange, Inward Rectifier Potassium Current, and Residual &bgr;-Adrenergic Responsiveness , 2001, Circulation research.

[85]  V Avdonin,et al.  A beta2 adrenergic receptor signaling complex assembled with the Ca2+ channel Cav1.2. , 2001, Science.

[86]  S. Ishiwata,et al.  Length Dependence of Tension Generation in Rat Skinned Cardiac Muscle: Role of Titin in the Frank-Starling Mechanism of the Heart , 2001, Circulation.

[87]  S. Marx,et al.  Phosphorylation-Dependent Regulation of Ryanodine Receptors , 2001, The Journal of cell biology.

[88]  S. Viatchenko‐Karpinski,et al.  Modulation of the Ca2+‐induced Ca2+ release cascade by β‐adrenergic stimulation in rat ventricular myocytes , 2001 .

[89]  S. Marx,et al.  Coupled Gating Between Cardiac Calcium Release Channels (Ryanodine Receptors) , 2001, Circulation research.

[90]  S. Howlett,et al.  Cardiac excitation-contraction coupling: role of membrane potential in regulation of contraction. , 2001, American journal of physiology. Heart and circulatory physiology.

[91]  D. Bers,et al.  When is cAMP not cAMP? Effects of compartmentalization. , 2001, Circulation research.

[92]  E. Lakatta,et al.  &bgr;-Adrenergic Stimulation Synchronizes Intracellular Ca2+ Release During Excitation-Contraction Coupling in Cardiac Myocytes , 2001, Circulation research.

[93]  J. Leiden,et al.  Phosphorylation of Troponin I by Protein Kinase A Accelerates Relaxation and Crossbridge Cycle Kinetics in Mouse Ventricular Muscle , 2001, Circulation research.

[94]  Length Dependence of Tension Generation in Rat Skinned Cardiac Muscle , 2001 .

[95]  Donald M. Bers,et al.  Na+-Ca2+ Exchange Current and Submembrane [Ca2+] During the Cardiac Action Potential , 2002, Circulation research.

[96]  Tong Zhang,et al.  Transgenic CaMKII&dgr;C Overexpression Uniquely Alters Cardiac Myocyte Ca2+ Handling: Reduced SR Ca2+ Load and Activated SR Ca2+ Release , 2003, Circulation research.

[97]  D. Bers,et al.  Elevated Sarcoplasmic Reticulum Ca2+ Leak in Intact Ventricular Myocytes From Rabbits in Heart Failure , 2003, Circulation research.

[98]  Donald M Bers,et al.  Cellular Basis of Abnormal Calcium Transients of Failing Human Ventricular Myocytes , 2003, Circulation research.

[99]  R. Sitsapesan,et al.  Regulation of the gating of the sheep cardiac sarcoplasmic reticulum ca2+-release channel by luminal Ca2+ , 1994, The Journal of Membrane Biology.