Yung Earm

Ionic Channels and Effect of Taurine on the Heart

Preface D. Noble. 1. Introduction to the Study and Role of Background Current Mechanisms in the Heart D. Noble, S.J. Noble, T. Kiyosue, A.J. Spindler. 2. Catecholamine-Induced Chloride Current in Cardiac Myocytes A. Noma, K. Ono, F.M. Tareen, M. Takano. 3. Modulation of the Atrial Muscarinic-Gated K Current by Phosphorylation Donghee Kim. 4. Intracellular Taurine, Intracellular Sodium and Defense against Cellular Damage R.A. Chapman, M.S. Suleiman, G.C. Rodrigo, K.K. Minezaki, K.R. Chatamra, C.R. Little, D.K. Misty, T.J.A. Allen. 5. Taurine Effects on Ion Channels of Cardiac Muscle N. Sperelakis, H. Satoh. 6. Effect of Taurine on the Activation of Background Current in Cardiac Myocytes of the Rabbit Y.E. Earm, W.K. Ho, I. So, C.H. Leem, J. Han. 7. Protective Effect of Taurine on the Failing Heart and its Clinical Application J. Azuma, S.W. Schaffer. 8. Concluding Remarks D. Noble. Index.

Effect of taurine on the activation of background current in cardiac myocytes of the rabbit

Several amino acids, such as taurine, aspartate, glutamate and β- alanine, are concentrated by cardiac cells up to very large concentrations, for instance, up to 30mM in the case of taurine (Huxtable, 1978). There are two important questions to be answered about these amino acids, especially taurine; how such a large gradient for taurine is established across the sarcolemmal membrane in the mammalian heart and for what it is used. In spite of this large gradient, taurine is not incorporated into proteins and is slowly metabolized with a half-life in the body of around 15 days (Huxtable, 1978). Taurine, however, has been shown to protect the heart from Ca-paradox (Kramer et al., 1981; Takihara et al., 1988), hypoxic injury (Franconi et al, 1985; Sawamura et al., 1986) and Na-overloading (Suleiman et al., 1992) and to have a beneficial effect on chronic congestive heart failure (Takihara et al., 1986).

Na-Ca Exchange Current During the Cardiac Action Potential

Action potentials recorded from rabbit atrial cells have two distinct phases: an initial spike of depolarization followed by a late low plateau. This late plateau is abolished in the presence of ryanodine (which blocks calcium release from the SR) or when external sodium is replaced by lithium ions. The fully activated current-voltage relationship of the plateau current displays a near exponential curve, characteristic of the sodium-calcium exchanger (Earm, Ho & So 1990). The ionic currents that flow during the action potential of an isolated rabbit atrial cell were reconstructed in a model developed by Earm and Noble (1990), based on the multicellular Hilgemann & Noble (1987) model. The separation between the calcium current, ICa, and the exchange current, INaCa is almost complete. The calcium current is rapidly deactivated once repolarization (initiated by the outward transient current) begins. The amount of calcium entering the cell via the voltage gated calcium channels is approximately equal to that which is extruded by the exchanger, and thus the intracellular calcium concentration returns to the resting level by the end of the action potential.