RyR-NCX-SERCA local cross-talk ensures pacemaker cell function at rest and during the fight-or-flight reflex

Circulation Research

Volumn 113, Issue 10, 2013, Pages

  Maltsev, Anna V ^a,b   Yaniv, Yael ^c   Stern, Michael D ^c   Lakatta, Edward G ^c   Maltsev, Victor A ^c  

^a UNIVERSITY OF BRISTOL   (United Kingdom)

^b Pace Biologics   (United States)

^c NATIONAL INSTITUTE ON AGING   (United States)

Author keywords

Calcium; Sarcoplasmic reticulum; Sinoatrial node; Sodium calcium exchanger

Indexed keywords

CALCIUM CHANNEL L TYPE; CALCIUM ION; CALCIUM RELEASE ACTIVATED CALCIUM CHANNEL; SARCOPLASMIC RETICULUM CALCIUM TRANSPORTING ADENOSINE TRIPHOSPHATASE;

ACTION POTENTIAL; AMPLITUDE MODULATION; ARTICLE; BETA ADRENERGIC STIMULATION; CALCIUM HOMEOSTASIS; CELL FUNCTION; CELLS; FLIGHT; HEART ARRHYTHMIA; HEART AUTOMATICITY; MATHEMATICAL MODEL; PRIORITY JOURNAL; REST; RESTING HEART RATE; SIMULATION; SINUS NODE; SODIUM CALCIUM EXCHANGE;

EID: 84887193890     PISSN: 00097330     EISSN: 15244571     Source Type: Journal    
DOI: 10.1161/CIRCRESAHA.113.302465     Document Type: Article

References (23)

1. Zhou Z, Lipsius SL. Na+-Ca2+ exchange current in latent pacemaker cells isolated from cat right atrium. J Physiol. 1993;466:263-285.
2. Hüser J, Blatter LA, Lipsius SL. Intracellular Ca2+ release contributes to automaticity in cat atrial pacemaker cells. J Physiol. 2000;524 Pt 2:415-422.
3. Bogdanov KY, Vinogradova TM, Lakatta EG. Sinoatrial nodal cell ryanodine receptor and Na+-Ca2+ exchanger: molecular partners in pacemaker regulation. Circ Res. 2001;88:1254-1258.
4. Sanders L, Rakovic S, Lowe M, Mattick PA, Terrar DA. Fundamental importance of Na+-Ca2+ exchange for the pacemaking mechanism in guineapig sino-atrial node. J Physiol. 2006;571:639-649.
5. Lakatta EG, Maltsev VA, Vinogradova TM. A coupled SYSTEM of intracellular Ca2+ clocks and surface membrane voltage clocks controls the timekeeping mechanism of the heart's pacemaker. Circ Res. 2010;106:659-673.
6. Gao Z, Rasmussen TP, Li Y, et al. Genetic inhibition of Na+-Ca2+ exchanger current disables fight or flight sinoatrial node activity without affecting resting heart rate. Circ Res. 2013;112:309-317.
7. Slodzinski MK, Blaustein MP. Na+/Ca2+ exchange in neonatal rat heart cells: antisense inhibition and protein half-life. Am J Physiol. 1998;275:C459-C467.
8. Herrmann S, Lipp P, Wiesen K, Stieber J, Nguyen H, Kaiser E, Ludwig A. The cardiac sodium-calcium exchanger NCX1 is a key player in the initiation and maintenance of a stable heart rhythm. Cardiovasc Res. 2013;99:780-788.
9. Groenke S, Larson ED, Nakano H, Nakano A, Proenza C, Philipson KD, Goldhaber JI. Atrial-specific NCX KO mice reveal dependence of sinoatrial node pacemaker activity on sodium-calcium exchange. Biophys J. 2012;102:663a.
10. Pott C, Henderson SA, Goldhaber JI, Philipson KD. Na+/Ca2+ exchanger knockout mice: plasticity of cardiac excitation-contraction coupling. Ann N Y Acad Sci. 2007;1099:270-275.
11. Kurata Y, Hisatome I, Imanishi S, Shibamoto T. Dynamical description of sinoatrial node pacemaking: improved mathematical model for primary pacemaker cell. Am J Physiol Heart Circ Physiol. 2002;283:H2074-H2101.
12. Severi S, Fantini M, Charawi LA, DiFrancesco D. An updated computational model of rabbit sinoatrial action potential to investigate the mechanisms of heart rate modulation. J Physiol. 2012;590:4483-4499.
13. Maltsev VA, Lakatta EG. Synergism of coupled subsarcolemmal Ca2+ clocks and sarcolemmal voltage clocks confers robust and flexible pacemaker function in a novel pacemaker cell model. Am J Physiol Heart Circ Physiol. 2009;296:H594-H615.
14. Luo CH, Rudy Y. A dynamic model of the cardiac ventricular action potential. I. Simulations of ionic currents and concentration changes. Circ Res. 1994;74:1071-1096.
15. Vinogradova TM, Lyashkov AE, Zhu W, et al. High basal protein kinase A-dependent phosphorylation drives rhythmic internal Ca2+ store oscillations and spontaneous beating of cardiac pacemaker cells. Circ Res. 2006;98:505-514.
16. Maltsev VA, Lakatta EG. A novel quantitative explanation for the autonomic modulation of cardiac pacemaker cell automaticity via a dynamic system of sarcolemmal and intracellular proteins. Am J Physiol Heart Circ Physiol. 2010;298:H2010-H2023.
17. Maltsev VA, Lakatta EG. Numerical models based on a minimal set of sarcolemmal electrogenic proteins and an intracellular Ca2+ clock generate robust, flexible, and energy-efficient cardiac pacemaking. J Mol Cell Cardiol. 2013;59:181-195.
18. Yaniv Y, Sirenko S, Ziman BD, Spurgeon HA, Maltsev VA, Lakatta EG. New evidence for coupled clock regulation of the normal automaticity of sinoatrial nodal pacemaker cells: Bradycardic effects of ivabradine are linked to suppression of intracellular Ca(2+) cycling. J Mol Cell Cardiol. 2013;62:80-89.
19. Maltsev AV, Maltsev VA, Mikheev M, Maltseva LA, Sirenko SG, Lakatta EG, Stern MD. Synchronization of stochastic Ca2+ release units creates a rhythmic Ca2+ clock in cardiac pacemaker cells. Biophys J. 2011;100:271-283.
20. Vinogradova TM, Zhou YY, Maltsev V, Lyashkov A, Stern M, Lakatta EG. Rhythmic ryanodine receptor Ca2+ releases during diastolic depolarization of sinoatrial pacemaker cells do not require membrane depolarization. Circ Res. 2004;94:802-809.
21. Stern MD. Theory of excitation-contraction coupling in cardiac muscle. Biophys J. 1992;63:497-517.
22. Vinogradova TM, Bogdanov KY, Lakatta EG. beta-Adrenergic stimulation modulates ryanodine receptor Ca2+ release during diastolic depolarization to accelerate pacemaker activity in rabbit sinoatrial nodal cells. Circ Res. 2002;90:73-79.
23. Torrente AG, Seinfeld J, Zhang R, Philipson KD, Goldhaber JI. Persistent periodic Ca2+ release in sinoatrial node of Na+-Ca2+ exchanger knockout mice. Biophys J. 2013;104:209a (Abstract).