Pyrethroids such as deltamethrin are widely used to control insect pests. Due to their selective toxicity to insects, they are considered harmless to birds and mammals. On the other hand, polycyclic aromatic hydrocarbons (PAHs) such as retene are widespread contaminants in aquatic ecosystems and more problematic to endothermic vertebrates. Both pyrethroids and PAHs might affect the developmental and functional processes in the cardiovascular system of fish. Therefore, deltamethrin and retene toxicity to the electrical excitability of ventricular myocytes were examined in the Oncorhynchus mykiss (rainbow trout) heart. Micromolar concentrations of deltamethrin and retene modified the action potential (AP) morphology in a time-dependent manner. After 5 min of application, both compounds strongly prolonged AP duration (APD) compared to control AP. However, deltamethrin prolonged APD by 42% and 25% more than retene at APD₅₀ and APD₉₀, respectively. In contrast, retene reduced APD₁₀ and the AP depolarization rate (+dV dt^-1) by 61% and 12% more than deltamethrin, respectively. Although deltamethrin and retene changed the ventricular AP shape in rainbow trout in the same way, their mechanism of action seems to be different. The findings revealed that deltamethrin mainly affects the outward potassium currents, while retene mainly affects the inward sodium and calcium currents. Further studies are needed to reveal the underlying ion currents/channels that might be involved in the AP attenuation of rainbow trout under the effect of deltamethrin and retene.