Polycyclic aromatic hydrocarbons phenanthrene and retene modify the action potential via multiple ion currents in rainbow trout Oncorhynchus mykiss cardiac myocytes

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous contaminants in aqueous environments. They affect cardiovascular development and function in fishes. The 3‐ring PAH phenanthrene has recently been shown to impair cardiac excitation–contraction coupling by inhibiting Ca2+ and K+ currents in marine warm‐water scombrid fishes. To see if similar events take place in a boreal freshwater fish, we studied whether the PAHs phenanthrene and retene (an alkylated phenanthrene) modify the action potential (AP) via effects on Na+ (INa), Ca2+ (ICaL), or K+ (IKr, IK1) currents in the ventricular myocytes of the rainbow trout (Oncorhynchus mykiss) heart. Electrophysiological characteristics of myocytes were measured using whole‐cell patch clamp. Micromolar concentrations of phenanthrene and retene modified the shape of the ventricular AP, and retene profoundly shortened the AP at low micromolar concentrations. Both PAHs increased INa and reduced ICaL and IKr, but retene was more potent. Neither of the PAHs had an effect on IK1. Our results show that phenanthrene and retene affect cardiac function in rainbow trout by a mechanism that involves multiple cardiac ion channels, and the final outcome of these changes (shortening of AP) is opposite to that observed in scombrid fishes (prolongation of AP). The results also show that retene and aryl hydrocarbon receptor (AhR) agonist have an additional mechanism of toxicity besides the previously known AhR‐mediated, transcription‐dependent one.