Cardiac actions of taurine on the ionic channel currents are as follows; (a) a prolongation of the action potential duration (APD) at high pCa and a shortening of APD at low pCa, (b) a stimulation of spontaneous activity at low extracellular Ca2+ concentrations, and vice versa, (c) an inhibition of the L-type Ca2+ current at high pCa, and vice versa, (d) a stimulation of the T- type Ca2+ current, (e) an inhibition of the fast Na+ current, (f) an enhancement of TTX-insensitive Na+ current, (g) an inhibition of the delayed rectifier K+ current at high pCa, and vice versa, (h) an enhancement of the transient outward current, (i) an inhibition of the ATP-sensitive K+ current, (j) an inhibition of the inwardly rectifying K+ currents, and (k) an inhibition/enhancement of the hyperpolarization-activated inward current. Finally, (1) taurine abolished some arrhythmias induced by a triggered activity under the conditions of cellular calcium overload. These results demonstrate that taurine could exert the potent cardioprotective actions involved with the modulation of ionic channels at low and high pCa levels, resulting in an antiarrhythmic actions. Therefore, taurine may be expected the possible therapeutic use of the sulphur amino acid.
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