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

• DOI: 10.1152/ajpregu.00349.2001
• Publication Date: 2015-03-03T20:24:04Z
• Authors: Matti Vornanen; Ari Ryökkynen; Antti Nurmi
• Keywords: 0301 basic medicine; Patch-Clamp Techniques; Potassium Channels; Acclimatization; Heart Ventricles; Myocardium; Muscle Fibers, Skeletal; Action Potentials; Body Temperature; Cold Temperature; 03 medical and health sciences; Sarcolemma; Barium; Potassium Channels, Voltage-Gated; Oncorhynchus mykiss; Potassium; Animals; Heart Atria; Delayed Rectifier Potassium Channels

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 ( IK1) and the E-4031-sensitive delayed rectifier current ( IKr). In atrial cells, the density of IK1is very low and the density of IKris remarkably high. The opposite is true for ventricular cells. Acclimation to cold (4°C) modified the two K+currents in opposite ways. Acclimation to cold increases the density of IKrand depresses the density of IK1. These changes in repolarizing K+currents alter the shape of the action potential, which is much shorter in cold-acclimated than warm-acclimated (17°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.