Temperature-dependent expression of sarcolemmal K+ currents in rainbow trout atrial and ventricular myocytes

Temperature has a strong influence on the excitability and the contractility of the ectothermic heart that can be alleviated in some species by temperature acclimation. The molecular mechanisms involved in the temperature-induced improvement of cardiac contractility and excitability are, however, still poorly known. The present study examines the role of sarcolemmal K+ currents from rainbow trout (Oncorhynchus mykiss) cardiac myocytes after thermal acclimation. The two major K+ conductances of the rainbow trout cardiac myocytes were identified as the Ba2+-sensitive background inward rectifier current (I-K1) and the E-4031-sensitive delayed rectifier current (I-Kr). In atrial cells, the density of I-K1 is very low and the density of I-Kr is remarkably high. The opposite is true for ventricular cells. Acclimation to cold (4degreesC) modified the two K+ currents in opposite ways. Acclimation to cold increases the density of I-Kr and depresses the density of I-K1. These changes in repolarizing K+ currents alter the shape of the action potential, which is much shorter in cold-acclimated than warm-acclimated (17degreesC) trout. These results provide the first concrete evidence that K+ channels of trout cardiac myocytes are adaptable units that provide means to regulate cardiac excitability and contractility as a function of temperature.