Objectives: 

Pyrethroids are extensively used for the control of insect pests and disease vectors but it is very toxic to fishes. This study tests the hypothesis that the piscine Na⁺ channels are more sensitive to a type II pyrethroid, deltamethrin (DM), than are the mammalian Na⁺ channels.

Materials and methods: 

Electrophysiology of single cells were conducted on enzymatically isolated ventricular myocytes by the patch-clamp methods. Cardiac action potentials (AP) were recorded by microelectrode methods in intact cardiac tissue. For measuring heart rate (HR) and force of atrial contraction were used sinoatrial preparations consisting of the sinus venosus and the whole atrium.

Results: 

In ventricular myocytes of the rainbow trout (Oncorhynchus mykiss) heart DM (10-7-10-5 M) modified Na⁺ current by slowing inactivation and shifting the reversal potential of the current to the left. Maximally 27 ± 4% of the cardiac Na⁺ channels were modified by DM and the half-maximal effect occurred at the concentration of 1.1 mM. The effect of DM on trout cardiac Na⁺ channels is stronger and occurs about an order of magnitude lower concentration in comparison to the orthologous mammalian Na⁺ channels. In sinoatrial preparations in vitro DM (10 mM) caused irregularities in rate, rhythm and force of atrial beating suggesting that DM is arrhythmogenic in the trout heart. Consistent with this, DM (>0.1 mM) induced spontaneous action potentials in otherwise quiescent ventricular myocytes.

Conclusions: 

These findings indicate that DM exerts toxic effects on trout heart, and suggest that the higher sensitivity of fishes to pyrethroid insecticides in comparison to mammals and birds is partially due to the higher affinity of their Na⁺ channels to pyrethroids.