Effects of seasonal acclimatization on thermal tolerance of inward currents in roach (Rutilus rutilus) cardiac myocytes

  title={Effects of seasonal acclimatization on thermal tolerance of inward currents in roach (Rutilus rutilus) cardiac myocytes},
  author={Ahmed Badr and Hanna Korajoki and El-Sabry Abu-Amra and M. F. El-Sayed and Matti Vornanen},
  journal={Journal of Comparative Physiology B},
To test the hypothesis of temperature-dependent deterioration of electrical excitability (TDEE) (Vornanen, J Exp Biol 219:1941–1952, 2016), the role of sodium (INa) and calcium (ICa) currents in heat tolerance of cardiac excitability was examined in a eurythermic fish, the roach (Rutilus rutilus). Densities of cardiac ICa and INa and their acute heat tolerance were measured in winter-acclimatized (WiR) and summer-acclimatized (SuR) fish maintained in the laboratory at 4 ± 1 and 18 ± 1 °C… 
Electrical excitability of roach ( Rutilus rutilus) ventricular myocytes: effects of extracellular K+, temperature, and pacing frequency.
Although high [K+]o antagonizes the negative effects of high temperature on excitation threshold, the precipitous depression of the rate of AP upstroke and complete loss of excitability in some myocytes suggest that the combination of highTemperature and high [ K+]O will severely impair ventricular excitabilityIn roach.
Cardiac Toxicity of Cadmium Involves Complex Interaction Between Multiple Ion Currents in Rainbow Trout (Oncorhynchus mykiss) Ventricular Myocytes.
Investigation of the effects of Cd2+ on ventricular action potentials and major ion currents in the rainbow trout ventricular myocytes indicates that the cardiotoxicity of C d2+ in fish involves multiple ion currents that are directly and indirectly altered by Cd 2+ .
Warmer, faster, stronger: Ca2+ cycling in avian myocardium
Avian cardiac cells have large SR stores and large sarcolemmal Ca2+ currents; these features may be the key to high performance of the avian heart despite their reptilian-like ultrastructure.
Depression of heart rate in fish at critically high temperatures is due to atrioventricular block
Findings show that at critically high temperatures AV block causes ventricular bradycardia which is an outcome from the increased excitation threshold of the ventricle due to changes in passive (resting ion leak) and active (inward charge movement) electrical properties of ventricular myocytes.
Atrioventricular block, due to reduced ventricular excitability, causes the depression of fish heart rate in fish at critically high temperatures.
Results show that at critically high temperatures AV block causes ventricular bradycardia which is an outcome from the increased excitation threshold of the ventricle due to changes in passive (resting ion leak) and active (inward charge movement) electrical properties of ventricular myocytes.
Feeling the heat: source–sink mismatch as a mechanism underlying the failure of thermal tolerance
  • M. Vornanen
  • Chemistry, Medicine
    Journal of Experimental Biology
  • 2020
A modified hypothesis about high temperature-induced failure of electrically excitable tissues is discussed, and can explain a number of heat-induced effects, including reduced heart rate, reduced synaptic transmission between neurons and reduced impulse transfer from neurons to muscles.
Phenanthrene alters the electrical activity of atrial and ventricular myocytes of a polar fish, the Navaga cod
The cardiotoxic effects exerted by phenanthrene on the atrium and ventricle of navaga cod are reported, the first data that is aware of on the impact of phen anthrene on atrial myocyte function in any fish species.
Reduced ventricular excitability causes atrioventricular block and depression of heart rate in fish at critically high temperatures
ABSTRACT At critically high temperature, cardiac output in fish collapses as a result of depression of heart rate (bradycardia). However, the cause of bradycardia remains unresolved. To investigate
Elevated cortisol lowers thermal tolerance but results in limited cardiac remodelling in rainbow trout (Oncorhynchus mykiss) experiencing chronic social stress.
High baseline cortisol levels in subordinate trout result in lowered thermal tolerance, but 5 d of social stress did not greatly affect cardiac structure and function, as previously reported for cortisol-treated rainbow trout.


Effects of seasonal acclimatization on action potentials and sarcolemmal K+ currents in roach (Rutilus rutilus) cardiac myocytes.
Findings show that thermal tolerance limits of K+ currents in isolated myocytes between seasonally acclimatized roach are much less pronounced than the heat sensitivity of ECG variables in intact fish.
Effects of seasonal acclimatization on temperature dependence of cardiac excitability in the roach, Rutilus rutilus
Seasonal acclimatization of the electrical excitability of the eurythermal roach increases pumping capacity of the roach heart by maximizing heart rate, but without compromising the stability of cardiac excitation.
Acute heat tolerance of cardiac excitation in the brown trout (Salmo trutta fario)
Findings from different levels of biological organization strongly suggest that heat-dependent deterioration of Na+ channel function disturbs normal spread of electrical excitation over the heart, leading to progressive variability of cardiac rhythmicity, reduction of heart rate and finally cessation of the normal heartbeat.
Temperature acclimation modifies Na+ current in fish cardiac myocytes
INa of fish cardiac myocytes shows thermal plasticity that is different in several respects in cold-dormant and cold-active species and thus has a physiologically meaningful role in supporting the variable life styles and habitat conditions of each species.
Seasonal changes of cholinergic response in the atrium of Arctic navaga cod (Eleginus navaga)
Testing the hypothesis that the ligand-gated K+ current, the acetylcholine-activated inward rectifier, IKACh, is also modified by seasonal acclimatization in atrial myocytes of navaga results in a drastic up-regulation of the atrial IKA Ch, which effectively shortens atrial AP.
Effects of prolonged anoxia on electrical activity of the heart in crucian carp (Carassius carassius)
Low temperature pre-conditions the crucian carp heart for prolonged anoxia by changes in activity of excitation–contraction coupling genes and thereby allows sustained bradycardia and prolongation of ventricular action potential when oxygen shortage sets in.
L-type Ca2+ current in fish cardiac myocytes: effects of thermal acclimation and beta-adrenergic stimulation.
  • M. Vornanen
  • Biology, Medicine
    The Journal of experimental biology
  • 1998
The patch-clamp analysis of L-type Ca2+ current in ventricular myocytes of cold- and warm-acclimated rainbow trout and crucian carp hearts concluded that sarcolemmal Ca2- current is not increased after acclimation to cold, and that ss-adrenergic stimulation of Ca2+.
Acute Temperature Change Modulates the Response of ICa to Adrenergic Stimulation in Fish Cardiomyocytes
It is suggested that the tonic level of adrenergic stimulation provided by circulating plasma catecholamines may be crucial for effective excitation‐contraction coupling in the cold cardiomyocyte.
Maximum heart rate in brown trout (Salmo trutta fario) is not limited by firing rate of pacemaker cells.
It is strongly suggested that the frequency generator of the sinoatrial pacemaker cells does not limit fH at high temperatures in the brown trout in vivo.
Ryanodine and dihydropyridine receptor binding in ventricular cardiac muscle of fish with different temperature preferences
There was a close correlation (r2=0.78) between the RyR/DHPR ratio and the magnitude of the Ry-sensitive component of contraction in ventricular muscle among the fish species examined in this study.