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 Ba(2+)-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 (4 degrees C) 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 (17 degrees C) 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.

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