Temperature acclimation modifies sinoatrial pacemaker mechanism of the rainbow trout heart (original) (raw)
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Journal of Experimental Biology
At critically high temperature, cardiac output in fish collapses due to depression of heart rate (bradycardia). However, the cause of bradycardia remains unresolved. To this end rainbow trout (Oncorhynchus mykiss; acclimated at +12°C) were exposed to acute warming, while electrocardiograms were recorded. From +12℃ to +25.3℃, electrical excitation between different parts of the heart was coordinated but above +25.3℃ atrial and ventricular beating rates became partly dissociated due to 2:1 atrioventricular (AV) block. With further warming atrial rate increased to the peak value of 188±22 bpm at +27℃, while the rate of the ventricle reached the peak value of 124±10 bpm at +25.3 ℃ and thereafter dropped to 111±15 bpm at +27℃. In single ventricular myocytes, warming from +12°C to +25°C attenuated electrical excitability as evidenced by increases in rheobase current and critical depolarization required to trigger action potential. The depression of excitability was caused by temperature i...
The Journal of experimental biology, 2016
Time course studies are critical for understanding regulatory mechanisms and temporal constraints in ectothermic animals acclimating to warmer temperatures. Therefore, we investigated the dynamics of heart rate and its neuro-humoral control in rainbow trout ( ITALIC! Onchorhynchus mykissL.) acclimating to 16°C for 39 days after being acutely warmed from 9°C. Resting heart rate was 39 beats min(-1)at 9°C, and increased significantly when fish were acutely warmed to 16°C ( ITALIC! Q10=1.9), but then declined during acclimation ( ITALIC! Q10=1.2 at day 39), mainly due to increased cholinergic inhibition while the intrinsic heart rate and adrenergic tone were little affected. Maximum heart rate also increased with warming, although a partial modest decrease occurred during the acclimation period. Consequently, heart rate scope exhibited a complex pattern with an initial increase with acute warming, followed by a steep decline and then a subsequent increase, which was primarily explained...
American Journal of …, 2008
Hassinen M, Haverinen J, Vornanen M. Electrophysiological properties and expression of the delayed rectifier potassium (ERG) channels in the heart of thermally acclimated rainbow trout. therms, compensatory changes in ion channel number and activity are needed to maintain proper cardiac function at variable temperatures. The rapid component of the delayed rectifier K ϩ current (IKr) is important for repolarization of cardiac action potential and, therefore, crucial for regulation of cellular excitability and heart rate. To examine temperature plasticity of cardiac I Kr, we cloned the ether-à-gogo-related gene (ERG) channel and measured its electrophysiological properties in thermally acclimated rainbow trout (Oncorhynchus mykiss; omERG). The present findings demonstrate a complete thermal compensation in the whole cell conductance of the atrial I Kr in rainbow trout acclimated to 4°C (cold acclimation) and 18°C (warm acclimation). In situ hybridization indicates that transcripts of the omERG channel are present throughout the muscular tissue of the heart, and quantitative PCR shows increased expression of the omERG in cold-acclimated trout compared with warm-acclimated trout. In both acclimation groups, omERG expression is higher in atrium than ventricle. In addition, the omERG has some functional features that support I Kr activity at low temperatures. Voltage dependence of steady-state activation is completely resistant to temperature changes, and steady-state inactivation and activation kinetics are little affected by temperatures below 11°C. Collectively, these findings suggest that high density of cardiac I Kr is achieved by cold-induced increase in the number of functional omERG channels and inherent insensitivity of the omERG to temperature below 11°C. These adaptations are probably important in maintaining high heart rates and proper excitability and contractility of trout cardiac myocytes in the cold.
Thermal plasticity of cardiorespiratory function allows ectotherms like fish to cope with seasonal temperature changes and is critical for resilience to climate change. Yet, the chronic thermal effects on cardiovascular homeostatic reflexes in fish are little understood although this may have important implications for physiological performance and overall resilience to climate warming. We compared cardiac autonomic control and baroreflex regulation of heart rate in perch (Perca fluviatilis L.) from a reference area in the Baltic Sea at 18–19°C with conspecifics from the Biotest enclosure, a chronically heated ecosystem receiving warmed effluent water (24–25°C) from a nuclear power plant. Resting heart rate of Biotest fish displayed clear thermal compensation and was 58.3±2.3 beats min −1 compared with 52.4±2.6 beats min −1 in reference fish at their respective environmental temperatures (Q 10 =1.2). The thermally compensated heart rate of Biotest fish was a combined effect of elevated inhibitory cholinergic tone (105% in Biotest fish versus 70% in reference fish) and reduced intrinsic cardiac pacemaker rate. A barostatic response was evident in both groups, as pharmacologically induced increases and decreases in blood pressure resulted in atropine-sensitive bradycardia and tachycardia, respectively. Yet, the tachycardia in Biotest fish was significantly greater, presumably due to the larger scope for vagal release. Acclimation of Biotest fish to 18°C for 3 weeks abolished differences in intrinsic heart rate and autonomic tone, suggesting considerable short-term thermal plasticity of cardiovascular control in this species. The heightened hypotensive tachycardia in Biotest perch may represent an important mechanism of ectothermic vertebrates that safeguards tissue perfusion pressure when tissue oxygen demand is elevated by environmental warming.
The temperature dependence of electrical excitability in fish hearts
The Journal of experimental biology, 2016
Environmental temperature has pervasive effects on the rate of life processes in ectothermic animals. Animal performance is affected by temperature, but there are finite thermal limits for vital body functions, including contraction of the heart. This Review discusses the electrical excitation that initiates and controls the rate and rhythm of fish cardiac contraction and is therefore a central factor in the temperature-dependent modulation of fish cardiac function. The control of cardiac electrical excitability should be sensitive enough to respond to temperature changes but simultaneously robust enough to protect against cardiac arrhythmia; therefore, the thermal resilience and plasticity of electrical excitation are physiological qualities that may affect the ability of fishes to adjust to climate change. Acute changes in temperature alter the frequency of the heartbeat and the duration of atrial and ventricular action potentials (APs). Prolonged exposure to new thermal condition...
Temperature Sensitivity of Cardiac Function in Pelagic Fishes
We measured the temperature sensitivity, adrenergic sensitivity, and dependence on sarcoplasmic reticulum (SR) Ca 2ϩ of ventricular muscle from pelagic fishes with different vertical mobility patterns: bigeye tuna (Thunnus obesus), yellowfin tuna (Thunnus albacares), and mahimahi (Coryphaena hippurus) and a single specimen from swordfish (Xiphias gladius). Ventricular muscle from the bigeye tuna and mahimahi exhibited a biphasic response to an acute decrease in temperature (from 26Њ to 7ЊC); twitch force and kinetic parameters initially increased and then declined. The magnitude of this response was larger in the bigeye tuna than in the mahimahi. Under steady state conditions at 26ЊC, inhibition of SR Ca 2ϩ release and reuptake with ryanodine and thapsigargin decreased twitch force and kinetic parameters, respectively, in the bigeye tuna only. However, the initial inotropy associated with decreasing temperature was abolished by SR inhibition in both the bigeye tuna and the mahimahi. Application of adrenaline completely reversed the effects of ryanodine and thapsigargin, but this effect was diminished at cold temperatures. In the yellowfin tuna, temperature and SR inhibition had minor effects on twitch force and kinetics, while adrenaline significantly increased these parameters. Limited data suggest that swordfish ventricular muscle responds to acute temperature reduction, SR inhibition, and adrenergic stimulation in a manner similar to that of bigeye tuna ventricular muscle. In aggregate, our results show that the temperature sensitivity, SR dependence, and adrenergic sensitivity of pelagic fish hearts are species specific and that these differences reflect species-specific vertical mobility patterns.
Temperature dependence of cardiac sarcoplasmic reticulum function in rainbow trout myocytes
The Journal of Experimental Biology, 2002
with 200 ms SQ pulses at the same frequencies (664±180 µmol l-1 Ca 2+ , 474±75 µmol l-1 Ca 2+ and 367±42 µmol l-1 Ca 2+ at 7°C, 14°C and 21°C, respectively). Also, and in contrast to 200 ms SQ pulse stimulation, temperature had little effect on steady-state SR Ca 2+ accumulation during AP stimulation. Furthermore, we observed SR-Ca 2+-dependent inactivation of the L-type Ca 2+ channel current (ICa) at 7°C, 14°C and 21°C, providing additional evidence of maintained SR function in fish hearts over an acute range of temperatures. We conclude that the waveform of the AP may be critical in ensuring adequate SR Ca 2+ cycling during temperature change in rainbow trout in vivo.