Abstract: AIM　The L-Type calcium currents were investigated in normal, hypertrophied and amiloride-treated rat ventricular myocytes so as to clarify the possible cause of the action potential lengthening that has been reported in thyroxine-induced hypertrophy. The interactions between agents such as thyroxine, Ang II and phenylephrine which induced hypertrophy with amiloride on the calcium current were analyzed. METHODS　Myocardial hypertrophy was induced by ip L-thyroxine in rats. The cell length, cell width and cell area were measured by image analysis technique. For recording I_CaL, the whole cell patch clamp technique was used. Potassium currents were suppressed by replacing K⁺ ions with Cs⁺ ions in intracellular media, and sodium current was blocked by 50 μmol.L^-1 tetrodotoxin. RESULTS　The Ca²⁺ current was found to be larger in hypertrophied cells (783pA) than in normal cells (433pA) and in amiloride-treated cells (429pA). However, no significant difference was observed in current density (6.54, 8.33, 5.74 pA/pF) in normal, hypertrophied and amiloride-treated cells. I_Ca displayed the same voltage dependence in three cell types. The potential giving 50% of activation (V_1/2) moved towards more negative and the slope of activation curve was smaller in hypertrophied cells than in normal cells and amiloride cells. When expressed as percentages, the maximal increases in I_Ca were obtained with 1 μmol.L^-1 Ang II and 100 μmol.L^-1 phenylephrine in normal cells (+45.5% and +81.8%). Thyroxine 100 μmol.L^-1 showed no effect on I_Ca. After giving amiloride, Ang II and phenylephrine did not increase the amplitude of I_Ca. CONCLUSION　At the dose of 0.5 mg.kg^-1.d^-1, amiloride (po) was shown to prevent the amplitude of I_Ca from increasing and to be effective against increases of amplitude of I_Ca by Ang II and phenylephrine.