Exercise, capture, and handling stress in fish can elevate extracellular K concentration ([K]) with potential impact on heart function in a temperature- and frequency-dependent manner. To this end, the effects of [K] on the excitability of ventricular myocytes of winter-acclimatized roach ( Rutilus rutilus) (4 ± 0.5°C) were examined at different test temperatures and varying pacing rates. Frequencies corresponding to in vivo heart rates at 4°C (0.37 Hz), 14°C (1.16 Hz), and 24°C (1.96 Hz) had no significant effect on the excitability of ventricular myocytes. Acute increase of temperature from 4 to 14°C did not affect excitability, but a further rise to 24 markedly decreased excitability: stimulus current and critical depolarization needed to elicit an action potential (AP) were ~25 and 14% higher, respectively, at 24°C than at 4°C and 14°C ( P < 0.05). This depression could be due to temperature-related mismatch between inward Na and outward K currents. In contrast, an increase of [K] from 3 to 5.4 or 8 mM at 24°C reduced the stimulus current needed to trigger AP. However, other aspects of excitability were strongly depressed by high [K]: maximum rate of AP upstroke and AP duration were drastically (89 and 50%, respectively) reduced at 8 mM [K] in comparison with 3 mM ( P < 0.05). As an extreme case, some myocytes completely failed to elicit all-or-none AP at 8 mM [K] at 24°C. Also, amplitude and overshoot of AP were reduced by elevation of [K] ( P < 0.05). Although high [K] 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 high temperature and high [K] will severely impair ventricular excitability in roach.

To test the hypothesis of temperature-dependent deterioration of electrical excitability (TDEE) (Vornanen, J Exp Biol 219:1941-1952, 2016), the role of sodium (I ) and calcium (I) currents in heat tolerance of cardiac excitability was examined in a eurythermic fish, the roach (Rutilus rutilus). Densities of cardiac I and I 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, respectively. A robust L-type Ca current (I ), but no T-type Ca current, was present in roach atrial and ventricular myocytes. Peak density of I was smaller in atrial (- 1.97 ± 0.14 and - 1.75 ± 0.19 pA/pF for WiR and SuR, respectively) than ventricular myocytes (- 4.00 ± 0.59 and - 2.88 ± 0.47 pA/pF for WiR and SuR, respectively) (p< 0.05), but current density and heat tolerance of I did not change between seasons in either cell type. In contrast to I, marked differences appeared in I between WiR and SuR. I density was 38% higher in WiR than SuR atrial myocytes (- 80.03 ± 5.92 vs. - 49.77 ± 4.72 pA/pF; p < 0.05) and 48% higher in WiR than SuR ventricular myocytes (- 39.25 ± 3.06 vs. - 20.03 ± 1.79 pA/pF; p < 0.05). The winter increase in I density was associated with 55% (1.70 ± 0.27 vs. 0.77 ± 0.12) and 54% (1.08 ± 0.19 vs. 0.50 ± 0.10) up-regulation of the total Na channel (scn4 + scn5 + scn8) transcripts in atrium and ventricle, respectively (p < 0.05). Heat tolerance of atrial I was lower in WiR with a breakpoint temperature of 20.3 ± 1.2 °C than in SuR (23.8 ± 0.7 °C) (p< 0.05). The response of I to seasonal acclimatization conforms to the TDEE hypothesis. The lower heat tolerance of I in WiR is consistent with the lower heat tolerance of in vivo heart rate in WiR in comparison to SuR, but the match is not quantitatively perfect, suggesting that other factors in addition to I may be involved.

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The present study was undertaken to examine the relative contribution of the SR-Ca 2+ release and sarcolemmal Ca 2+ channels in developing the cardiac force at two different temperatures (20 and 30°C) in the catfish (Clarias gariepinus).The sarcolemmal Ca 2+ contribution of activator Ca 2+ was greater at a test temperature of 30°C as assessed by verapamil. Whereas the SR-Ca 2+ contribution was higher at 20 and 30°C and a frequency rate of 0.2 and 0.4 Hz as assessed by caffeine and adrenaline, respectively. Bradykinin potentiating factor (BPF 7 ) which was isolated from jelly fish (Cassiopea andromeda) decreased the cardiac force developed at a frequency rate of 0.2 Hz and a temperature of 20°C, whereas it increased the force developed at frequency rates of 0.2 and 0.4 Hz at 30°C. These results indicate that BPF 7 may act like verapamil in reducing the cardiac force through blocking the sarcolemmal Ca 2+ channels at low temperature and like adrenaline in an increase of the cardiac force developed at warm temperature and the high frequency rate through stimulation of SR-Ca 2+ activator. Therefore, this study indicates that the sarcolemmal Ca 2+ influx and the SR-Ca 2+ release contributors of activator Ca 2+ for cardiac force development in the catfish heart were significantly greater at warm temperature and at the pacing frequency rates of 0.2 and 0.4 Hz as assessed by verapamil, adrenaline, caffeine and BPF 7 . However, the relative contribution of the sarcolemmal Ca 2+ influx in the development of cardiac force in the catfish heart was greater than that of SR-Ca 2+ release. ª 2015 The Egyptian German Society for Zoology. Production and hosting by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).