scholarly journals Electrical excitability of roach (Rutilus rutilus) ventricular myocytes: effects of extracellular K+, temperature, and pacing frequency

2018 ◽  
Vol 315 (2) ◽  
pp. R303-R311 ◽  
Author(s):  
Ahmed Badr ◽  
El-Sabry Abu-Amra ◽  
Mohamed F. El-Sayed ◽  
Matti Vornanen
Keyword(s):  
High Temperature ◽  
Ventricular Myocytes ◽  
Heart Function ◽  
Rutilus Rutilus ◽  
Excitation Threshold ◽  
Dependent Manner ◽  
Roach Rutilus Rutilus ◽  
Handling Stress ◽  
Stimulus Current ◽  
High K

Exercise, capture, and handling stress in fish can elevate extracellular K+ concentration ([K+]o) with potential impact on heart function in a temperature- and frequency-dependent manner. To this end, the effects of [K+]o 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+]o 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+]o: maximum rate of AP upstroke and AP duration were drastically (89 and 50%, respectively) reduced at 8 mM [K+]o 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+]o at 24°C. Also, amplitude and overshoot of AP were reduced by elevation of [K+]o ( P < 0.05). 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 high temperature and high [K+]o will severely impair ventricular excitability in roach.

scholarly journals Depression of heart rate in fish at critically high temperatures is due to atrioventricular block

2020 ◽  
Author(s):  
Jaakko Haverinen ◽  
Matti Vornanen
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
High Temperature ◽  
Cardiac Function ◽  
High Temperatures ◽  
Ventricular Myocytes ◽  
Mechanistic Explanation ◽  
Excitation Threshold ◽  
Av Block ◽  
Peak Value

ABSTRACTAt critically high temperature, cardiac output in fish collapses due to depression of heart rate (bradycardia). However, the cause of bradycardia remains unresolved. Here we provide a mechanistic explanation for the temperature induced bradycardia. To this end rainbow trout (Oncorhynchus mykiss; acclimated at +12°C) were exposed to acute warming, while cardiac function was followed from electrocardiograms. From +12°C to +25.3°C, electrical excitation between different parts of the heart was coordinated but above +25.3°C 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°C, while the rate of the ventricle reached the peak value of 124 ± 10 bpm at +25.3°C and thereafter dropped to 111 ± 15 bpm at +27°C. 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 induced decrease in input resistance (sarcolemmal K+ leak via the outward IK1 current) of resting myocytes and decrease in inward charge transfer by the Na+ current (INa) of active myocytes. Collectively these 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. The sequence of events from the level of ion channels to the cardiac function in vivo provides a mechanistic explanation for the depression of cardiac output in fish at critically high temperature.

Population Characteristics and Feeding of Roach Rutilus rutilus in Small Regulated River of the Kyiv Polissya

2020 ◽  
Vol 56 (1) ◽  
pp. 42-48
Author(s):  
Ye. A. Gupalo ◽  
I. I. Abramyuk ◽  
S. A. Afanasyev ◽  
O. V. Manturova ◽  
Ye. V. Savchenko
Keyword(s):  
Rutilus Rutilus ◽  
Population Characteristics ◽  
Regulated River ◽  
Roach Rutilus Rutilus

scholarly journals Investigation into Adaptation in Genes Associated with Response to Estrogenic Pollution in Populations of Roach (Rutilus rutilus) Living in English Rivers

2020 ◽  
Vol 54 (24) ◽  
pp. 15935-15945
Author(s):  
Patrick B. Hamilton ◽  
Anne E. Lockyer ◽  
Tamsyn M. Uren Webster ◽  
David J. Studholme ◽  
Josephine R. Paris ◽  
...  
Keyword(s):  
Rutilus Rutilus ◽  
Roach Rutilus Rutilus

scholarly journals Molecular detection of a novel cyprinid herpesvirus in roach (Rutilus rutilus) and asp (Leuciscus aspius) showing typical signs of carp pox disease

2020 ◽  
Vol 165 (7) ◽  
pp. 1569-1576 ◽  
Author(s):  
Boglárka Sellyei ◽  
Ferenc Baska ◽  
Ádám Varga ◽  
Réka Borzák ◽  
Andor Doszpoly
Keyword(s):  
Molecular Detection ◽  
Rutilus Rutilus ◽  
Roach Rutilus Rutilus

Role of extracellular calcium and calmodulin in prolactin secretion induced by hyposmolarity, thyrotropin-releasing hormone, and high K+ in GH4C1 cells

1990 ◽  
Vol 123 (2) ◽  
pp. 218-224 ◽  
Author(s):  
Xiangbing Wang ◽  
Noriyuki Sato ◽  
Monte A. Greer ◽  
Susan E. Greer ◽  
Staci McAdams
Keyword(s):  
Smooth Muscle ◽  
Muscle Relaxant ◽  
Prolactin Secretion ◽  
Thyrotropin Releasing Hormone ◽  
Dependent Manner ◽  
Cell Toxicity ◽  
High K ◽  
Dose Dependent ◽  
Smooth Muscle Relaxant

Abstract. The mechanism by which 30% medium hyposmolarity induces PRL secretion by GH4C1 cells was compared with that induced by 100 nmol/l TRH or 30 mmol/l K+. Removing medium Ca2+, blocking Ca2+ channels with 50 μmol/l verapamil, or inhibiting calmodulin activation with 20 μmol/l trifluoperazine, 10 μmol/l chlorpromazine or 10 μmol/l pimozide almost completely blocked hyposmolarity-induced secretion. The smooth muscle relaxant, W-7, which is believed relatively specific in inhibiting the Ca2+-calmodulin interaction, depressed hyposmolarity-induced PRL secretion in a dose-dependent manner (r = −0.991, p<0.01 ). The above drugs also blocked or decreased high K+-induced secretion, but had much less effect on TRH-induced secretion. Secretion induced by TRH, hyposmolarity, or high K+ was optimal at pH 7.3-7.65 and was significantly depressed at pH 6.0 or 8.0, indicating that release of hormone induced by all 3 stimuli is due to an active cell process requiring a physiologic extracellular pH and is not produced by nonspecific cell toxicity. The data suggest hyposmolarity and high K+ may share some similarities in their mechanism of stimulating secretion, which is different from that of TRH.

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