Denis V. Abramochkin, Jaakko Haverinen, Yuri A. Mitenkov, and Matti Vornanen
Electrical excitability (EE) is vital for cardiac function and strongly modulated by temperature and external K+ concentration ([K+]o) as formulated in the hypothesis of temperature-dependent deterioration of electrical excitability (TDEE). Since little is known about EE of arctic stenothermic fishes, we tested the TDEE hypothesis on ventricular myocytes of polar cod (Boreogadus saida) and navaga cod (Eleginus navaga) of the Arctic Ocean and those of temperate freshwater burbot (Lota lota). Ventricular action potentials (APs) were elicited in current-clamp experiments at 3, 9 and 15°C, and AP characteristics and the current needed to elicit AP were examined. At 3°C, ventricular APs of polar and navaga cod were similar but differed from that of burbot in having lower rate of AP upstroke and higher rate of repolarization. EE of ventricular myocytes – defined as the ease with which all-or-none APs are triggered – was little affected by acute temperature changes between 3 and 15°C in any species. However, AP duration (APD50) was drastically reduced at higher temperatures. Elevation of [K+]o from 3 to 5.4 and further to 8 mM at 3, 9 and 15°C strongly affected EE and AP characteristics in polar and navaga cod, but less in burbot. In all species, ventricular excitation was resistant to acute temperature elevations, while small increases in [K+]o severely compromised EE, in particular in the marine stenotherms. This suggests that EE of the heart in these Gadiformes species is well equipped against acute warming, but less so against the simultaneous temperature and exercise stresses.