Cold adaptation suppresses the contractility of both atrial and ventricular muscle of the crucian carp heart

Abstract

Adaptation to low temperature in crucian carp Carasius carassius increases twitch duration both in atrial and ventricular muscle and the response is largely explained by a temperatureinduced reduction in myofibrillar ATPase activity. The prolonged twitch increases the refractoriness of both atrial and ventricular muscle, i.e. the optimal force development is achieved at longer diastolic intervals after acclimation to cold. The contractions of atrial and ventricular muscle are insensitive to 10  ryanodine, an inhibitor of SR release Ca 2+ channel but sensitive to 20  verapamil, a blocker of L-type Ca 2+ channels. This suggests that E-C-coupling in the crucian carp heart is exclusively based on extracellular Ca 2+ sources. The present findings indicate that cold-acclimation slows the contraction kinetics of the crucian carp heart and thereby preconditions the cardiac muscle for a low energy supply during winter anoxic conditions. 2001 The Fisheries Society of the British Isles

Temperature dependence of cardiac sarcoplasmic reticulum Ca2+-ATPase from rainbow trout Oncorhynchus mykiss

“…In fish hearts, extracellular Ca 2+ entry through the L-type sarcolemma (SL) channel is generally the major source of Ca 2+ used during cardiac contraction Tiitu & Vornanen, 2001). The SR, however, can play an important role during fish cardiac E-C coupling in some more active tunas, e.g.…”

Thermal acclimation and seasonal acclimatization: a comparative study of cardiac response to prolonged temperature change in shorthorn sculpin

“…Statistically significant differences between: summer-acclimated and winter-acclimatized groups (*P<0.05, **P<0.01, ***P<0.001, ****P<0.0001); winter-acclimatized groups and cold-acclimated groups ( # P<0.05, #### P<0.0001); summer-acclimated and cold-acclimated groups ( ‡ P<0.05). Vornanen, 1992;Pelouch and Vornanen, 1996;Tiitu and Vornanen, 2001;Vornanen, 1994;Vornanen et al, 1998). This remodelling resets the chronotropic (Aho and Vornanen, 2001;Haverinen and Vornanen, 2007) and inotropic (Aho and Vornanen, 1999;Tiitu and Vornanen, 2001) output of the fish heart, presumably to compensate the direct effects of temperature.…”

“…Vornanen, 1992;Pelouch and Vornanen, 1996;Tiitu and Vornanen, 2001;Vornanen, 1994;Vornanen et al, 1998). This remodelling resets the chronotropic (Aho and Vornanen, 2001;Haverinen and Vornanen, 2007) and inotropic (Aho and Vornanen, 1999;Tiitu and Vornanen, 2001) output of the fish heart, presumably to compensate the direct effects of temperature. Many of the studies (listed above) which have investigated thermal remodelling in fish hearts have used animals acclimated in the laboratory to a number of temperatures.…”

“…We did not measure oxygen content in the sea pens that held the winter-acclimatized fish. However, reduced activity and lowered metabolic rate (Hanson et al, 2008;Stehlik, 2009), reduced brain function (Vornanen and Paajanen, 2006), modified gill structure (Sollid et al, 2003), and reduced cardiac function (Aho and Vornanen, 1999;Matikainen and Vornanen, 1992;Tiitu and Vornanen, 2001) are all associated with hypoxia and anoxia in fishes. Whether the oxygen content in winter could drive seasonal changes that have downstream effects on the electrophysiological phenotype of fish heart would be worthy of investigation in the future.…”

Ca2+cycling in cardiomyocytes from a high-performance reptile, the varanid lizard (Varanus exanthematicus)

“…High resting and maximal heart rates in mammals have been associated with enhanced expression of an intracellular store of Ca 2+ , the sarcoplasmic reticulum (SR) ( 22 ). In most ectothermic vertebrates, the SR is poorly developed and the amount of Ca 2+ used for contraction originating from the SR is negligible ( 10 , 16 , 23 , 37 , 45 ). However, highly active species of fish with high heart rates and blood pressures, such as tuna, are more SR dependent than sedentary species ( 17 , 28 , 36 , 38 , 42 ).…”