Regulation of cardiac contractility in a cold stenothermal fish, the burbot Lota lota L.

In the present study, burbot (Lota lota L.) was used as a model to study the effects of acute temperature changes on cardiac contractility in a cold stenothermal fish. The burbot were captured in the breeding season (February) and were maintained for 4 weeks at 1-2 degrees C in the laboratory before the contractile properties of the heart were measured. Both isometric force and the pumping capacity of in vitro perfused hearts were maximum at the acclimation temperature (1 degrees C) and declined markedly when the temperature increased. At 1 degrees C heart rate was 25 beats min(-1) and increased to a maximum of 72 beats min(-1) at 18 degrees C, above which atrio-ventricular block was observed. Ryanodine (10 micromol l(-1)), an inhibitor of sarcoplasmic reticulum (SR) Ca2+ release channels, reduced the maximum developed force of paced atrial and ventricular preparations at 1 degrees C by 32+/-8 % and 16+/-3 %, respectively. At 7 degrees C, ryanodine-induced inhibition of force increased to 52+/-3 % and 44+/-5 % in the atrium and ventricle, respectively. At 1 degrees C, ryanodine abolished rest-potentiation and turned it into rest-decay in both atrial and ventricular muscle. Ryanodine, however, had no effect on the mechanical refractory period or on the rate constants of mechanical and relaxation restitution in either preparation at 1 degrees C. The activity of myofibrillar Ca2+Mg2+-ATPase was higher in atrial than ventricular muscle and the temperature optimum of the ATPase in vitro was approximately 10 degrees C in both preparations. Our results indicate a significant dependence on SR Ca2+ stores for contractile activation in the burbot heart at temperatures that are known to inhibit SR function in mammalian heart. This suggests that the ryanodine receptors of the teleost heart, unlike those of the endotherms, are not leaky as temperatures approach 0 degrees C. Reliance on SR Ca2+ stores in both cold stenothermal burbot and cold-acclimated eurythermal teleosts suggests that enhanced SR Ca2+-release is a common characteristic of cold-living fish and may improve cardiac contractility in the cold.