Role of Individual Ionic Current Systems in the SA Node Hypothesized by a Model Study

Sarai, Nobuaki; Matsuoka, Satoshi; Kuratomi, Shinobu; Ono, Koichi; Noma, Akinori

doi:10.2170/jjphysiol.53.125

Cited by 69 publications

(46 citation statements)

References 39 publications

(43 reference statements)

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“…In the Kyoto Model developed by Sarai et al (17), conductance and kinetics of I CaT measured in rabbit SAN I CaT were incorporated, and spontaneous action potentials of SAN cells were well reconstructed (17). In a typical SAN cell, net current carried at the pacemaker potential is inward and approximately 5 pA in amplitude.…”

Section: Contribution Of Tcc To Cardiac Pacemakingmentioning

confidence: 99%

Pathophysiological Significance of T-type Ca2+ Channels: Properties and Functional Roles of T-type Ca2+ Channels in Cardiac Pacemaking

Ono

Iwamoto

2005

J Pharmacol Sci

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Abstract. Calcium channels are essential for excitation-contraction coupling and pacemaker activity in cardiac myocytes. While L-type Ca 2+ channels (LCC) have been extensively studied, functional roles of T-type channels (TCC) in native cardiac myocytes are still debatable. TCC are activated at more negative membrane potentials than LCC and therefore facilitate slow diastolic depolarization in sinoatrial node cells. Recent studies showed that selective inhibition of TCC produced a marked slowing of the pacemaker rhythm, indicating that contribution of TCC to cardiac automaticity was relatively larger than what had been speculated in previous studies. To re-evaluate TCC, we measured current density and kinetics of TCC in sinoatrial node cells of various mammalian species. Current density of TCC was larger in mice and guinea pigs than in rabbit and porcine sinoatrial node cells. Interestingly, few or no obvious TCC were recorded in porcine sinoatrial node cells. Furthermore, it was demonstrated that TCC could be enhanced by several vasoactive substances, thereby increasing spontaneous firing rate of sinoatrial node cells. TCC may, at least in part, account for different heart rates among various mammalian species. In addition, TCC might be involved in physiological and / or pathophysiological modulations of the heart rate.

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Section: Contribution Of Tcc To Cardiac Pacemakingmentioning

confidence: 99%

Pathophysiological Significance of T-type Ca2+ Channels: Properties and Functional Roles of T-type Ca2+ Channels in Cardiac Pacemaking

Ono

Iwamoto

2005

J Pharmacol Sci

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“…An alternative approach to study the phase and frequency dependency is the use of numerical modeling. We modeled the optically-controlled beating dynamics of heart muscle cells by simultaneous differential equations, based on perturbations to a modified form heart muscle cell model based on the sinoatrial node KYOTO model (Sarai et al, 2003). The KYOTO model represents different type of cells (adult rat sinoatrial node) from the one we used in experiments.…”

Section: Modeling Of the Pacemaker Effectmentioning

confidence: 99%

Optical Techniques for Future Pacemaker Technology

Kumamoto¹,

Smith²,

Fujita³

et al. 2011

Modern Pacemakers - Present and Future

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“…In this model, a mathematical representation of the cell elements that are responsible for membrane excitation, the intracellular ion concentration changes, and contraction (such as the plasmalemmal ion channels and transporters and the sarcoplasmic reticulum) are essentially the same as our previous cardiac cell model (Kyoto model) [27,28]. The description of cardiac myocyte shortening is based on a 4-state model [29].…”

Section: A Simple Model Of Excitation-contraction-atp Metabolism Coupmentioning

confidence: 99%

An <i>In Silico</i> Study of Energy Metabolism in Cardiac Excitation-Contraction Coupling

Matsuoka

Sarai

et al. 2004

Jpn.J.Physiol

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developed a computer model of cardiac excitation-contraction coupling (Kyoto model) that includes the major processes of ATP production, such as oxidative phosphorylation that was originally developed for skeletal muscle by Korzeniewski and Zoladz [Biophys Chem 92: 17-34, 2001], creatine kinase, and adenylate kinase. In this review, we briefly summarize cardiac energy metabolism and discuss the regulation of mitochondrial ATP synthesis, using the Kyoto model. Energy balance is a key issue in cellular homeostasis, how it is achieved and what the consumers and producers of energy are. The problem of energy balance has been studied by the development of computer models of relatively simple cell types, such as the red blood cells and Escherichia coli (see review by Bassingthwaighte [1]). The next step in these studies is an in silico analysis of the energy homeodynamics of cardiac muscle, in which the major consumers of energy, such as muscle contraction and ion pumping, have been well studied. The basic principles required for modeling energy balance are summarized by Bassingthwaighte [1] and Jafri et al. [2]. Heart muscle receives energy from substrates and oxygen and delivers energy mainly for pumping blood around the systemic and pulmonary systems. The chemical energy that supports this cardiac work is derived from the hydrolysis of ATP. Therefore the heart is an energy transducer. An estimation based on myocardial oxygen consumption indicated that the human heart produces 35 kg of ATP in one day, which is more than 100 times its own weight and more than 10,000 times the amount of ATP it stores [3]. Thus the heart produces and uses ATP at an extremely high rate. Each step associated with ATP metabolism has been extensively studied. The relationship between ATP production and membrane excitation-contraction coupling, however, which is a main ATP-consuming process, is not yet fully understood because of complicated interactions and the lack of quantitative data in vivo. Computer simulation is a powerful tool with which to integrate experimental data and to solve the complicated interactions. But only a few computer models have been developed to deal with the cardiac excitation-contraction-energy metabolism coupling [4]. In this review we briefly summarize cardiac energy metabolism and describe our recent studies about cardiac ATP metabolism.

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Role of Individual Ionic Current Systems in the SA Node Hypothesized by a Model Study

Cited by 69 publications

References 39 publications

Pathophysiological Significance of T-type Ca2+ Channels: Properties and Functional Roles of T-type Ca2+ Channels in Cardiac Pacemaking

Pathophysiological Significance of T-type Ca2+ Channels: Properties and Functional Roles of T-type Ca2+ Channels in Cardiac Pacemaking

Optical Techniques for Future Pacemaker Technology

An <i>In Silico</i> Study of Energy Metabolism in Cardiac Excitation-Contraction Coupling

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