Permissive action of thyroid hormone at the level of Ca channel and responsible mechanisms underlying thyroid hormone-induced change in myocardial contractile state and T₃-induced arrhythmias were investigated in rabbit ventricular or atrial myocytes using whole cell patch clamp technique. Single cells were isolated by Langendorff perfusion with collagenase. Cardiac myocytes were incubated in low-Cl^-,, high-K⁺ medium containing 1_μM L-triiodothyronine (T₃) at 4℃ for 2.10 hours. The calcium currrent (I_Ca) was increased in T₃ loaded cells, however, the shape of current voltage curve and reverse potential did not altered. Cyclic AMP, cyclic GMP, isoprenaline and 3-isobutyl-1-methyl-xanthine increased I_Ca in euthyroid and hyperthyroid conditions, and acetylcholine blocked the increase of I_Ca in T₃ loaded cells. The amplitude of I_Ca was much larger after perfusing cGMP than cGMP in both conditions, whereas the degree of increase of I_Ca was greater after perfusing cAMP than cGMP in T₃ loaded cells. The degree of increase of I_Ca after perfusing isoprenaline or IBMX also was greater in T₃ loaded cells than in control cells. Background current induced by isoprenaline also increased in T₃ loaded cells. The Ca release dependent inward current was increased in amplitude but its activation and inactivation time course was not changed in T₃ loaded cells. Activation of Na pump current was not changed in T₃ loaded cells. From the above results it is suggested that thyroid hormone induced increase in the contractile state of cardiac myocytes are accompanied by augmented I_Ca and the increase of Ca release from sarcoplasmic reticulum and the permissive action of thyroid hormone to catecholamines could induce arrhythmias through the increase of I_Ca and background current.