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Journal of Molecular and Cellular Cardiology
Volume 47, Issue 2
, Pages 157-170
, August 2009
What keeps us ticking: a funny current, a calcium clock, or both?
References
- . Ivabradine for patients with stable coronary artery disease and left-ventricular systolic dysfunction (BEAUTIFUL): a randomised, double-blind, placebo-controlled trial. Lancet. 2008;372:807–816
- . How does adrenaline accelerate the heart?. Nature. 1979;280:235–236
- . The cardiac hyperpolarizing-activated current, if. Origins and developments. Prog. Biophys. Mol. Biol. 1985;46:163–183
- . Pacemaker mechanisms in cardiac tissue. Annu. Rev. Physiol. 1993;55:455–472
- . Physiology and pharmacology of the cardiac pacemaker (“funny”) current. Pharmacol. Ther. 2005;107:59–79
- . Control of cardiac rate by “funny” channels in health and disease. Ann. N. Y. Acad. Sci. 2008;1123:213–223
- . Effect of current flow on the membrane potential of cardiac muscle. J. Physiol. 1951;115:227–236
- . Analysis of cardiac pacemaker potential using a “voltage clamp” technique. Am. J. Physiol. 1966;210:1335–1341
- . The kinetics and rectifier properties of the slow potassium current in cardiac Purkinje fibres. J. Physiol. 1968;195:185–214
- . Adrenaline: mechanism of action on the pacemaker potential in cardiac Purkinje fibers. Science. 1968;162:916–917
- . The effects of calcium on outward membrane currents in the cardiac Purkinje fibre. J. Physiol. 1979;289:347–373
- . The effects of potassium and temperature on the pace-maker current, iK2, in Purkinje fibres. J. Physiol. 1976;260:55–74
- . A new interpretation of the pace-maker current in calf Purkinje fibres. J. Physiol. 1981;314:359–376
- . A study of the ionic nature of the pace-maker current in calf Purkinje fibres. J. Physiol. 1981;314:377–393
- . Properties of the current if in the sino-atrial node of the rabbit compared with those of the current iK, in Purkinje fibres. J. Physiol. 1980;308:353–367
- . Properties of the hyperpolarizing-activated current (if) in cells isolated from the rabbit sino-atrial node. J. Physiol. 1986;377:61–88
- . Acetylcholine inhibits activation of the cardiac hyperpolarizing-activated current, if. Pflugers. Arch. 1987;410:139–142
- . Inhibition of the hyperpolarization-activated current (if) induced by acetylcholine in rabbit sino-atrial node myocytes. J. Physiol. 1988;405:477–491
- . Muscarinic control of the hyperpolarization-activated current (if) in rabbit sino-atrial node myocytes. J. Physiol. 1988;405:493–510
- . Acetylcholine activation of single muscarinic K+ channels in isolated pacemaker cells of the mammalian heart. Nature. 1983;303:250–253
- . Muscarinic modulation of cardiac rate at low acetylcholine concentrations. Science. 1989;243:669–671
- . Direct activation of cardiac pacemaker channels by intracellular cyclic AMP. Nature. 1991;351:145–147
- . Regulation of cardiac L-type calcium current by phosphorylation and G proteins. Annu. Rev. Physiol. 1990;52:257–274
- . Localization of f-channels to caveolae mediates specific beta2-adrenergic receptor modulation of rate in sinoatrial myocytes. J. Mol. Cell. Cardiol. 2007;42:71–78
- . Differential targeting of beta-adrenergic receptor subtypes and adenylyl cyclase to cardiomyocyte caveolae. A mechanism to functionally regulate the cAMP signaling pathway. J. Biol. Chem. 2000;275:41447–41457
- . beta(2)-Adrenergic receptor signaling complexes in cardiomyocyte caveolae/lipid rafts. J. Mol. Cell. Cardiol. 2004;37:407–415
- . Cardiac pacemaking in the sinoatrial node. Physiol. Rev. 1993;73:197–227
- . Modulation of single hyperpolarization-activated channels (i(f)) by cAMP in the rabbit sino-atrial node. J. Physiol. 1994;474:473–482
- . Modulation of cyclic nucleotide-regulated HCN channels by PIP(2) and receptors coupled to phospholipase C. Pflugers. Arch. 2007;455:125–145
- Distribution and prevalence of hyperpolarization-activated cation channel (HCN) mRNA expression in cardiac tissues. Circ. Res. 1999;85:e1–e6
- Differential expression of ion channel transcripts in atrial muscle and sinoatrial node in rabbit. Circ. Res. 2006;99:1384–1393
- . Organisation of the mouse sinoatrial node: structure and expression of HCN channels. Cardiovasc. Res. 2007;73:729–738
- . Expression of the hyperpolarization-activated cyclic nucleotide-gated cation channel HCN4 during mouse heart development. Gene. Expr. Patterns. 2003;3:777–783
- Extended atrial conduction system characterised by the expression of the HCN4 channel and connexin45. Cardiovasc. Res. 2006;72:271–281
- . Developmental change in the voltage-dependence of the pacemaker current, if, in rat ventricle cells. Pflugers. Arch. 1997;433:533–535
- I(f) current and spontaneous activity in mouse embryonic ventricular myocytes. Circ. Res. 2001;88:536–542
- . Characterization of the hyperpolarization-activated current, I(f), in ventricular myocytes isolated from hypertensive rats. J. Physiol. 1994;481(Pt 3)):585–591
- Tbx3 controls the sinoatrial node gene program and imposes pacemaker function on the atria. Genes. Dev. 2007;21:1098–1112
- . Influence of postnatal-development on I(f) occurrence and properties in neonatal rat ventricular myocytes. Cardiovasc. Res. 1999;42:416–423
- . Hyperpolarization-activated inward current in ventricular myocytes from normal and failing human hearts. Circulation. 1998;97:55–65
- The properties of the pacemaker current I(F)in human ventricular myocytes are modulated by cardiac disease. J. Mol. Cell. Cardiol. 2001;33:441–448
- . Regional distribution of hyperpolarization-activated current (If) and hyperpolarization-activated cyclic nucleotide-gated channel mRNA expression in ventricular cells from control and hypertrophied rat hearts. J. Physiol. 2003;553:395–405
- . Expression of the hyperpolarization-activated current, I(f), in cultured adult rat ventricular cardiomyocytes and its modulation by hypertrophic factors. Pharmacol. Res. 2008;57:100–109
- Pacemaker channel dysfunction in a patient with sinus node disease. J. Clin. Invest. 2003;111:1537–1545
- Functional characterization of a trafficking-defective HCN4 mutation, D553N, associated with cardiac arrhythmia. J. Biol. Chem. 2004;279:27194–27198
- . Familial sinus bradycardia associated with a mutation in the cardiac pacemaker channel. N. Engl. J. Med. 2006;354:151–157
- Point mutation in the HCN4 cardiac ion channel pore affecting synthesis, trafficking, and functional expression is associated with familial asymptomatic sinus bradycardia. Circulation. 2007;116:463–470
- . Cardiovascular actions of N-allyl-clonidine (ST 567), a substance with specific bradycardic action. Eur. J. Pharmacol. 1979;58:141–150
- . On the mechanism of the “specific bradycardic action” of the verapamil derivative UL-FS 49. Naunyn-Schmiedeberg's Arch. Pharmacol. 1990;341:331–340
- . Use- and frequency-dependent blockade by UL-FS 49 of the if pacemaker current in sheep cardiac Purkinje fibres. Eur. J. Pharmacol. 1990;187:241–256
- . Current-dependent block of rabbit sino-atrial node I(f) channels by ivabradine. J. Gen. Physiol. 2002;120:1–13
- . Heart rate lowering by specific and selective I(f) current inhibition with ivabradine: a new therapeutic perspective in cardiovascular disease. Drugs. 2004;64:1757–1765
- . HCN2 overexpression in newborn and adult ventricular myocytes: distinct effects on gating and excitability. Circ. Res. 2001;89:E8–14
- . Biological pacemaking: a concept whose time has come...or is coming. Heart. 2007;93:145–146
- . Experimental molecular and stem cell therapies in cardiac electrophysiology. Ann. N. Y. Acad. Sci. 2008;1123:224–231
- Expression and function of a biological pacemaker in canine heart. Circulation. 2003;107:1106–1109
- Biological pacemaker implanted in canine left bundle branch provides ventricular escape rhythms that have physiologically acceptable rates. Circulation. 2004;109:506–512
- Adenoviral gene transfer of HCN4 creates a genetic pacemaker in pigs with complete atrioventricular block. Life Sci. 2007;80:1746–1753
- Human mesenchymal stem cells as a gene delivery system to create cardiac pacemakers. Circ. Res. 2004;94:952–959
- Electromechanical integration of cardiomyocytes derived from human embryonic stem cells. Nat. Biotechnol. 2004;22:1282–1289
- . Genes, stem cells and biological pacemakers. Cardiovasc. Res. 2004;64:12–23
- Single cells isolated from human sinoatrial node: action potentials and numerical reconstruction of pacemaker current. Conf. Proc. IEEE. Eng. Med. Biol. Soc. 2007;904–907
- . The electrophysiological properties of spontaneously beating pacemaker cells isolated from mouse sinoatrial node. J. Physiol. 2003;550:169–180
- . Does the “pacemaker current” generate the diastolic depolarization in the rabbit SA node cells?. Pflugers Arch. 1983;397:190–194
- . Pacemaking in rabbit isolated sino-atrial node cells during Cs+ block of the hyperpolarization-activated current if. J. Physiol. 1990;429:401–409
- . Mechanisms of adrenergic control of sino-atrial node discharge. J. Biomed. Sci. 2003;10:179–192
- . Novel perspectives on the beating rate of the heart. Circ. Res. 2002;91:e3
- . HCN4 provides a ‘depolarization reserve’ and is not required for heart rate acceleration in mice. EMBO J. 2007;26:4423–4432
- Tamoxifen-inducible gene deletion in the cardiac conduction system. J. Mol. Cell. Cardiol. 2008;45:62–69
- . 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. 2009;296:H594–615
- . Computer modelling of the sinoatrial node. Med. Biol. Eng. Comput. 2007;45:189–207
- . Sino-atrial nodal cells of mammalian hearts: ionic currents and gene expression of pacemaker ionic channels. J. Smooth Muscle Res. 2003;39:175–193
- . Excitation–contraction coupling of the mouse embryonic cardiomyocyte. J. Gen. Physiol. 2008;132:397–405
- . Mathematical model of mouse embryonic cardiomyocyte excitation–contraction coupling. J. Gen. Physiol. 2008;132:407–419
- . Intracellular Ca2+ oscillations, a potential pacemaking mechanism in early embryonic heart cells. J. Gen. Physiol. 2007;130:133–144
- . How does beta-adrenergic stimulation increase the heart rate? The role of intracellular Ca2+ release in amphibian pacemaker cells. J. Physiol. 1999;516(Pt 3)):793–804
- . Synchrony dynamics during initiation, failure, and rescue of the segmentation clock. Science. 2007;317:1911–1915
- Coupling diurnal cytosolic Ca2+ oscillations to the CAS-IP3 pathway in Arabidopsis. Science. 2007;315:1423–1426
- . Inspiratory bursts in the preBotzinger complex depend on a calcium-activated non-specific cation current linked to glutamate receptors in neonatal mice. J. Physiol. 2007;582:113–125
- A mathematical model of pacemaker activity recorded from mouse small intestine. Philos. Transact. A Math. Phys. Eng. Sci. 2006;364:1135–1154
- . Pacemaking through Ca2+ stores interacting as coupled oscillators via membrane depolarization. Biophys. J. 2007;92:3843–3861
- . Hysteresis and bistability in a realistic cell model for calcium oscillations and action potential firing. Phys. Rev. Lett. 2007;098107:98
- Ca(2+)-stimulated basal adenylyl cyclase activity localization in membrane lipid microdomains of cardiac sinoatrial nodal pacemaker cells. J. Biol. Chem. 2008;283:14461–14468
- . Cesium effects on i(f) and i(K) in rabbit sinoatrial node myocytes: implications for SA node automaticity. J. Cardiovasc. Pharmacol. 1998;32:783–790
- . 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
- The hyperpolarization-activated channel HCN4 is required for the generation of pacemaker action potentials in the embryonic heart. Proc. Natl. Acad. Sci. U. S. A. 2003;100:15235–15240
- . Ionic basis of the chronotropic effect of acetylcholine on the rabbit sinoatrial node. Cardiovasc. Res. 1995;29:867–878
- Role of acetylcholine-activated potassium current (IKAch), hyperpolarization-activated current (If), Protein Kinase A (PKA)-dependent phosphorylation and Ca2+cycling in muscarinic receptor (M2R) regulation of spontaneous Action Potential Rate (APR) in isolated rabbit Sinoatrial Node Cells (SANC). Biophys. J. 2008;(Suppl. 251):(Abstract)
- Constitutive phosphodiesterase activity restricts spontaneous beating rate of cardiac pacemaker cells by suppressing local Ca2+ releases. Circ. Res. 2008;102:761–769
- Intracellular calcium dynamics and acceleration of sinus rhythm by beta-adrenergic stimulation. Circulation. 2009;119:788–796
- Crucial role of the sarcoplasmic reticulum in the developmental regulation of Ca2+ transients and contraction in cardiomyocytes derived from embryonic stem cells. FASEB J. 2006;20:181–183
- The ryanodine receptor modulates the spontaneous beating rate of cardiomyocytes during development. Proc. Natl. Acad. Sci. U. S. A. 2002;99:9225–9230
- 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
- . Effect of isoprenaline, carbachol, and Cs+ on Na+ activity and pacemaker potential in rabbit SA node cells. Am. J. Physiol. 1999;276:H205–H214
- . Ca2+-stimulated adenylyl cyclase isoform AC1 is preferentially expressed in guinea-pig sino-atrial node cells and modulates the If pacemaker current. J. Physiol. 2007;582:1195–1203
- Sinoatrial node pacemaker activity requires Ca2+/calmodulin-dependent protein kinase II activation. Circ. Res. 2000;87:760–767
- . Sinoatrial nodal cell ryanodine receptor and Na+–Ca2+ exchanger: molecular partners in pacemaker regulation. Circ. Res. 2001;88:1254–1258
- High basal cAMP content markedly elevates PKA-dependent protein phosphorylation and sustains spontaneous beating in rabbit sinoatrial nodal pacemaker cells (SANC). Biophys. J. 2006;90:155a;(Abstract)
- . I(f)-dependent modulation of pacemaker rate mediated by cAMP in the presence of ryanodine in rabbit sino-atrial node cells. J. Mol. Cell. Cardiol. 2003;35:905–913
- . Fundamental importance of Na+–Ca2+ exchange for the pacemaking mechanism in guinea-pig sino-atrial node. J. Physiol. 2006;571:639–649
- Targeted inactivation of the sodium–calcium exchanger (Ncx1) results in the lack of a heartbeat and abnormal myofibrillar organization. FASEB J. 2001;15:1209–1211
- . Embryonic lethality and abnormal cardiac myocytes in mice lacking ryanodine receptor type 2. EMBO J. 1998;17:3309–3316
- . Correlation between electrical activity and the size of rabbit sino-atrial node cells. J. Physiol. 1996;496(Pt 3):795–808
- . Variation in effects of Cs+, UL-FS-49, and ZD-7288 within sinoatrial node. Am. J. Physiol. 1997;272:H2782–H2792
- Role of pacemaking current in cardiac nodes: insights from a comparative study of sinoatrial node and atrioventricular node. Prog. Biophys. Mol. Biol. 2008;96:294–304
- . Expressional analysis of the cardiac Na–Ca exchanger in rat development and senescence. Cardiovasc. Res. 1998;37:405–423
- Reduced sinoatrial cAMP content plays a role in postnatal heart rate slowing in the rabbit. Clin. Exp. Pharmacol. Physiol. 2006;33:757–762
- . Reciprocal role of the inward currents ib, Na and i(f) in controlling and stabilizing pacemaker frequency of rabbit sino-atrial node cells. Proc. Biol. Sci. 1992;250:199–207
- . Bradycardic and proarrhythmic properties of sinus node inhibitors. Mol. Pharmacol. 2006;69:1328–1337
- Expanding spectrum of human RYR2-related disease: new electrocardiographic, structural, and genetic features. Circulation. 2007;116:1569–1576
- . Sinoatrial block in lithium toxicity. Am. J. Psychiatry. 2007;164:831–832
- . Cancer as a robust system: implications for anticancer therapy. Nat. Rev. Cancer. 2004;4:227–235
- . Excitation–Contraction Coupling and Cardiac Contractile Force. 2nd ed.. Kluwer Academic Publishers: Norwell, Mass; 2001;
- . Cyclic variation of intracellular calcium: a critical factor for cardiac pacemaker cell dominance. Circ. Res. 2003;92:e45–e50
- . Dynamic interactions of an intracellular Ca2+ clock and membrane ion channel clock underlie robust initiation and regulation of cardiac pacemaker function. Cardiovasc. Res. 2008;77:274–284
- . Ryanodine alteration of the contractile state of rat ventricular myocardium. Comparison with dog, cat, and rabbit ventricular tissues. Circ. Res. 1980;46:332–343
- . Ionic basis of ryanodine's negative chronotropic effect on pacemaker cells isolated from the sinoatrial node. Am. J. Physiol. 1997;273:H2481–H2489
- . Localisation and functional significance of ryanodine receptors during beta-adrenoceptor stimulation in the guinea-pig sino-atrial node. Cardiovasc. Res. 2000;48:254–264
- . Possible role of calcium release from the sarcoplasmic reticulum in pacemaking in guinea-pig sino-atrial node. Exp. Physiol. 1996;81:877–880
- . Mechanisms of automaticity in subsidiary pacemakers from cat right atrium. Circ. Res. 1989;64:648–657
- . Electrophysiological actions of ryanodine on single rabbit sinoatrial nodal cells. Gen. Pharmacol. 1997;28:31–38
- . Na+–Ca2+ exchange current in latent pacemaker cells isolated from cat right atrium. J. Physiol. 1993;466:263–285
- . Intracellular calcium and Na+–Ca2+ exchange current in isolated toad pacemaker cells. J. Physiol. 1998;508(Pt 1):153–166
- Calcium cycling protein density and functional importance to automaticity of isolated sinoatrial nodal cells are independent of cell size. Circ. Res. 2007;100:1723–1731
- . Intracellular Ca2+ and pacemaking within the rabbit sinoatrial node: heterogeneity of role and control. J. Physiol. 2004;556:481–494
- Heterogeneous expression of Ca2+ handling proteins in rabbit sinoatrial node. J. Histochem. Cytochem. 2002;50:311–324
- . Intracellular Ca2+ release contributes to automaticity in cat atrial pacemaker cells. J. Physiol. 2000;524(Pt 2):415–422
- Membrane potential fluctuations resulting from submembrane Ca2+ releases in rabbit sinoatrial nodal cells impart an exponential phase to the late diastolic depolarization that controls their chronotropic state. Circ. Res. 2006;99:979–987
- . Diastolic calcium release controls the beating rate of rabbit sinoatrial node cells: numerical modeling of the coupling process. Biophys. J. 2004;86:2596–2605
- . Rhythmic ryanodine receptor Ca2+ releases during diastolic depolarization of sinoatrial pacemaker cells do not require membrane depolarization. Circ. Res. 2004;94:802–809
- . Modulation of rate by autonomic agonists in SAN cells involves changes in diastolic depolarization and the pacemaker current. J. Mol. Cell. Cardiol. 2007;43:39–48
- High basal Ca2+/calmodulin kinase II activity modulates spontaneous sarcoplasmic reticulum Ca2+ cycling that drives normal automaticity in sinoatrial nodal cells. Circulation. 2007;116:II_86–II_87
- . Differences in sarcoplasmic reticulum Ca2+ loading and spontaneous Ca2+ release in permeabilized sinoatrial nodal and ventricular myocytes: effect of cAMP. American Heart Association Meeting. Circulation. 2007;116:II_85;(Abstract)
- . Basal phosphorylation of Ca2+ cycling proteins by both PKA and CAMKII is required for robust generation of local subsarcolemmal Ca2+ releases to drive sinoatrial node cell automaticity. Circulation. 2008;118(Suppl. 2):S346
- . The emergence of a general theory of the initiation and strength of the heartbeat. J. Pharmacol. Sci. 2006;100:338–369
- . Beyond Bowditch: the convergence of cardiac chronotropy and inotropy. Cell. Calcium. 2004;35:629–642
- . Basal PKA-dependent protein phosphorylation contributes to generation of spontaneous action potentials in cardiomyocytes derived from mouse embryonic stem cells. Biophys. J. 2007;461a;Supplement: (Abstract)
- . Crosstalk between muscarinic receptor stimulation and PKA signaling in modulation of local submembrane calcium releases and beating rate of rabbit sinoatrial nodal cells. Biophys. J. 2005;1462;Supplement: Pos (Abstract)
- . Genesis and regulation of the heart automaticity. Physiol. Rev. 2008;88:919–982
- . Unlocking the secrets of cell signaling. Annu. Rev. Physiol. 2005;67:1–21
- Mutations in the cardiac ryanodine receptor gene (hRyR2) underlie catecholaminergic polymorphic ventricular tachycardia. Circulation. 2001;103:196–200
- Bidirectional ventricular tachycardia and fibrillation elicited in a knock-in mouse model carrier of a mutation in the cardiac ryanodine receptor. Circ. Res. 2005;96:e77–e82
PII: S0022-2828(09)00144-8
doi: 10.1016/j.yjmcc.2009.03.022
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Journal of Molecular and Cellular Cardiology
Volume 47, Issue 2
, Pages 157-170
, August 2009
