Cardiac activity of the fish heart is compromised at high temperatures and involves failure of underlying ion channel function. INa is the most heat sensitive of the major ion currents that contribute to initiation and propagation of the action potential. Heat tolerance of sarcolemmal ion channel function was explored to assess the role of adrenaline in the thermal tolerance of INa. Whole-cell patch clamp experiments were used to assess the role of adrenaline and the prolongation of INa thermal scope at high temperatures. At 21°C adrenaline induced a significant increase in voltage dependence of inactivation of the INa channels (one way ANOVA P<0.005, N=22) and both voltage dependence availability was shifted in the hyperpolarizing direction (-6.5±2.1mV). Furthermore, maximum conductance did not change, indicating a change only in channel kinetics. At 28°C, the current was diminished and subsequently revived with addition of 1μM adrenaline. These findings suggest that adrenaline has a protective role on cardiac activity and increases the functional thermal scope of INa, reducing heat sensitivity of the cardiomyocyte.