scholarly journals Effect of thermal acclimation on action potentials and sarcolemmal K+ channels from Pacific bluefin tuna cardiomyocytes

2009 ◽  
Vol 297 (2) ◽  
pp. R502-R509 ◽  
Author(s):  
G. L. J. Galli ◽  
M. S. Lipnick ◽  
B. A. Block
Keyword(s):  
Ventricular Myocytes ◽  
Bluefin Tuna ◽  
Thermal Acclimation ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Acclimation Temperature ◽  
Pacific Bluefin Tuna ◽  
Cold Temperatures ◽  
Wide Range ◽  
Effects Of Temperature

To sustain cardiac muscle contractility relatively independent of temperature, some fish species are capable of temporarily altering excitation-contraction coupling processes to meet the demands of their environment. The Pacific bluefin tuna, Thunnus orientalis, is a partially endothermic fish that inhabits a wide range of thermal niches. The present study examined the effects of temperature and thermal acclimation on sarcolemmal K+ currents and their role in action potential (AP) generation in bluefin tuna cardiomyocytes. Atrial and ventricular myocytes were enzymatically isolated from cold (14°C)- and warm (24°C)-acclimated bluefin tuna. APs and current-voltage relations of K+ channels were measured using the whole cell current and voltage clamp techniques, respectively. Data were collected either at the cardiomyocytes' respective acclimation temperature of 14 or 24°C or at a common test temperature of 19°C (to reveal the effects of acclimation). AP duration (APD) was prolonged in cold-acclimated (CA) cardiomyocytes tested at 14°C compared with 19°C and in warm-acclimated (WA) cardiomyocytes tested at 19°C compared with 24°C. This effect was mirrored by a decrease in the density of the delayed-rectifier current ( IKr), whereas the density of the background inward-rectifier current ( IK1) was unchanged. When CA and WA cardiomyocytes were tested at a common temperature of 19°C, no significant effects of temperature acclimation on AP shape or duration were observed, whereas IKr density was markedly increased in CA cardiomyocytes. IK1 density was unaffected in CA ventricular myocytes but was significantly reduced in CA atrial myocytes, resulting in a depolarization of atrial resting membrane potential. Our results indicate the bluefin AP is relatively short compared with other teleosts, which may allow the bluefin heart to function at cold temperatures without the necessity for thermal compensation of APD.

The Effects of Acclimation Temperature on a Neuromuscular System of the Crayfish, Astacus Leptodactylus

1979 ◽  
Vol 78 (1) ◽  
pp. 281-293
Author(s):  
MIKKO HARRI ◽  
ERNST FLOREY
Keyword(s):  
Membrane Lipids ◽  
Characteristic Temperature ◽  
Resting Membrane Potential ◽  
Acclimation Temperature ◽  
Muscle Fibres ◽  
Astacus Leptodactylus ◽  
Tension Development ◽  
Temperature Range ◽  
Wide Range ◽  
Warm Acclimation

1. Crayfish, Astacus leptodactylus, were acclimated to 12 °C and to 25 °C. Nerve muscle preparations (closer muscle of walking legs) were subjected to temperatures ranging from 6 to 32 °C. 2. The resting membrane potential of muscle fibres was found to increase with temperature in a linear manner, but with a change in slope at around 170 in cold-acclimated preparations, and around 24 °C in warm-acclimated ones. 3. Temperature acclimation shifted the temperature range of maximal amplitudes of fast and slow e.j.p.s toward the acclimation temperature. Optimal facilitation of slow e.j.p.s also occurred near the respective acclimation temperature. 4. E.j.p. decay time is nearly independent of temperature in the upper temperature range but increases steeply when the temperature falls below a critical range around 17 °C in preparations from cold-acclimated animals, and around 22 °C after acclimation to 25 °C. 5. Peak depolarizations reached by summating facilitated e.j.p.s are conspicuously independent of temperature over a wide range (slow and fast e.j.p.s of cold-acclimated preparations, fast e.j.p.s of warm-acclimated ones) which extends to higher temperatures after warm acclimation in the case of fast e.j.p.s. In warm-acclimated preparations the peak depolarization of slow e.j.p.s first falls then rises and falls again as the temperature increases from 8 to 32 °C. 6. Tension development elicited by stimulation of the slow axon at a given frequency reaches maximal values at the lower end of the temperature range in cold-acclimated preparations. The maximum is shifted towards 20 °C after warm acclimation. Fast contractions decline with temperature; possible acclimation effects are masked by the great lability of fast contractions in warm-acclimated preparations. 7. It is suggested that changes in the composition of membrane lipids may be responsible for the effects of acclimation on the electrical parameters and their characteristic temperature dependence.

Thermal Acclimation of a Central Neurone of Helix Aspersa: II. Electrophysiological Recordings

1979 ◽  
Vol 78 (1) ◽  
pp. 187-200
Author(s):  
C. K. LANGLEY
Keyword(s):  
Input Resistance ◽  
Helix Aspersa ◽  
Thermal Acclimation ◽  
Resting Membrane Potential ◽  
Acclimation Temperature ◽  
Simple Relationship ◽  
Electrophysiological Recordings ◽  
Acclimation Period ◽  
Block Temperature ◽  
Increasing Temperature

1. The effects of thermal acclimation on the activity of a central autoactive neurone and its temperature dependence were investigated in Helix aspersa. 2. Resting membrane potential was changed by acclimation temperature, but not with a simple relationship: cells from both 30°C-acclimated and 4°C-acclimated groups were more depolarized at 20°C than were control cells (acclimated to 19°C). 3. The input resistance of the neurone decreased as the temperature of acclimation was raised. 4. Rates of change of potential during an action potential decreased with increasing acclimation temperature. Raising the temperature of measurement on the other hand increased dV/dt at a given acclimation temperature. Spike amplitude was little affected. 5. The frequency of spontaneous spike discharge at a given temperature declined with increasing temperature of acclimation but increased with step changes of temperature in a manner suggestive of a compensatory process. 6. All the measured electrical parameters showed a pronounced hysteresis during rewarming after cold block. 7. Upper lethal and cold block temperatures were both significantly raised by acclimation to higher temperatures. Block temperature was much reduced in cold-acclimated individuals, but the upper lethal temperature was less affected. 8. By sampling during the acclimation period of 4 weeks, the above changes were shown to occur progressively. During the initial stages (5–12 days) they could be partially reversed by incubating isolated ganglia at various temperatures for 30-45 min: but after 2 weeks or more the changes could not be reversed by incubations of up to 5 h.

Tamoxifen inhibits Na+ and K+ currents in rat ventricular myocytes

2003 ◽  
Vol 285 (2) ◽  
pp. H661-H668 ◽  
Author(s):  
Jianying He ◽  
Margaret E. Kargacin ◽  
Gary J. Kargacin ◽  
Christopher A. Ward
Keyword(s):  
Membrane Potential ◽  
Ventricular Myocytes ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Rat Ventricular Myocytes ◽  
Life Threatening ◽  
Prolonged Qt Interval ◽  
Electrophysiological Mechanism ◽  
K Currents ◽  
Arrhythmogenic Effects

Tamoxifen is an estrogen receptor antagonist used in the treatment of breast cancer. However, tamoxifen has been shown to induce QT prolongation of the electrocardiogram, thereby potentially causing life-threatening polymorphic ventricular arrhythmias. The purpose of the present study was to elucidate the electrophysiological mechanism(s) that underlie the arrhythmogenic effects of tamoxifen. We used standard ruptured whole cell and perforated patch-clamping techniques on rat ventricular myocytes to investigate the effects of tamoxifen on cardiac action potential (AP) waveforms and the underlying K+ currents. Tamoxifen (3 μmol/l) markedly prolonged AP duration, decreased maximal rate of depolarization, and decreased resting membrane potential. At this concentration, tamoxifen significantly depressed the Ca2+-independent transient outward K+ current ( Ito), sustained outward delayed rectifier K+ current ( Isus), inward rectifier K+ current ( IK1), and Na+ current ( INa) in the myocytes. Lower concentrations of tamoxifen (1 μmol/l) also decreased the resting membrane potential and significantly depressed IK1 to 79 ± 5% ( n = 5; at –120 mV) of pretreatment values. The results of this study indicate that inhibition of Ito, Isus, and IK1 by tamoxifen may underlie AP prolongation in cardiac myocytes and thereby contribute to prolonged QT interval observed in patients.

scholarly journals Cardiac function in an endothermic fish: cellular mechanisms for overcoming acute thermal challenges during diving

2015 ◽  
Vol 282 (1800) ◽  
pp. 20141989 ◽  
Author(s):  
H. A. Shiels ◽  
G. L. J. Galli ◽  
B. A. Block
Keyword(s):  
Temperature Change ◽  
Ventricular Myocytes ◽  
Bluefin Tuna ◽  
Adrenergic Stimulation ◽  
Cellular Mechanisms ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Wide Range ◽  
Enhanced Expression ◽  
Cardiac Excitation

Understanding the physiology of vertebrate thermal tolerance is critical for predicting how animals respond to climate change. Pacific bluefin tuna experience a wide range of ambient sea temperatures and occupy the largest geographical niche of all tunas. Their capacity to endure thermal challenge is due in part to enhanced expression and activity of key proteins involved in cardiac excitation–contraction coupling, which improve cardiomyocyte function and whole animal performance during temperature change. To define the cellular mechanisms that enable bluefin tuna hearts to function during acute temperature change, we investigated the performance of freshly isolated ventricular myocytes using confocal microscopy and electrophysiology. We demonstrate that acute cooling and warming (between 8 and 28°C) modulates the excitability of the cardiomyocyte by altering the action potential (AP) duration and the amplitude and kinetics of the cellular Ca 2+ transient. We then explored the interactions between temperature, adrenergic stimulation and contraction frequency, and show that when these stressors are combined in a physiologically relevant way, they alter AP characteristics to stabilize excitation–contraction coupling across an acute 20°C temperature range. This allows the tuna heart to maintain consistent contraction and relaxation cycles during acute thermal challenges. We hypothesize that this cardiac capacity plays a key role in the bluefin tunas' niche expansion across a broad thermal and geographical range.

scholarly journals Characterization of two distinct depolarization-activated K+ currents in isolated adult rat ventricular myocytes.

1991 ◽  
Vol 97 (5) ◽  
pp. 973-1011 ◽  
Author(s):  
M Apkon ◽  
J M Nerbonne
Keyword(s):  
Steady State ◽  
Ventricular Myocytes ◽  
Outward Current ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Patch Clamp Recording ◽  
Rat Ventricular Myocytes ◽  
Adult Rat ◽  
Steady State Inactivation ◽  
K Currents

Depolarization-activated outward K+ currents in isolated adult rat ventricular myocytes were characterized using the whole-cell variation of the patch-clamp recording technique. During brief depolarizations to potentials positive to -40 mV, Ca(2+)-independent outward K+ currents in these cells rise to a transient peak, followed by a slower decay to an apparent plateau. The analyses completed here reveal that the observed outward current waveforms result from the activation of two kinetically distinct voltage-dependent K+ currents: one that activates and inactivates rapidly, and one that activates and inactivates slowly, on membrane depolarization. These currents are referred to here as Ito (transient outward) and IK (delayed rectifier), respectively, because their properties are similar (although not identical) to these K+ current types in other cells. Although the voltage dependences of Ito and IK activation are similar, Ito activates approximately 10-fold and inactivates approximately 30-fold more rapidly than IK at all test potentials. In the composite current waveforms measured during brief depolarizations, therefore, the peak current predominantly reflects Ito, whereas IK is the primary determinant of the plateau. There are also marked differences in the voltage dependences of steady-state inactivation of these two K+ currents: IK undergoes steady-state inactivation at all potentials positive to -120 mV, and is 50% inactivated at -69 mV; Ito, in contrast, is insensitive to steady-state inactivation at membrane potentials negative to -50 mV. In addition, Ito recovers from steady-state inactivation faster than IK: at -90 mV, for example, approximately 70% recovery from the inactivation produced at -20 mV is observed within 20 ms for Ito; IK recovers approximately 25-fold more slowly. The pharmacological properties of Ito and IK are also distinct: 4-aminopyridine preferentially attenuates Ito, and tetraethylammonium suppresses predominantly IK. The voltage- and time-dependent properties of these currents are interpreted here in terms of a model in which Ito underlies the initial, rapid repolarization phase of the action potential (AP), and IK is responsible for the slower phase of AP repolarization back to the resting membrane potential, in adult rat ventricular myocytes.

Electrophysiological response of rat ventricular myocytes to acidosis

2002 ◽  
Vol 283 (1) ◽  
pp. H412-H422 ◽  
Author(s):  
Kimiaki Komukai ◽  
Fabien Brette ◽  
Caroline Pascarel ◽  
Clive H. Orchard
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Ventricular Myocytes ◽  
Resting Potential ◽  
Disulfonic Acid ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Patch Clamp Technique ◽  
Electrophysiological Response ◽  
Inwardly Rectifying

The effects of acidosis on the action potential, resting potential, L-type Ca2+( I Ca), inward rectifier potassium ( I K1), delayed rectifier potassium ( I K), steady-state ( I SS), and inwardly rectifying chloride ( I Cl,ir) currents of rat subepicardial (Epi) and subendocardial (Endo) ventricular myocytes were investigated using the patch-clamp technique. Action potential duration was shorter in Epi than in Endo cells. Acidosis (extracellular pH decreased from 7.4 to 6.5) depolarized the resting membrane potential and prolonged the time for 50% repolarization of the action potential in Epi and Endo cells, although the prolongation was larger in Endo cells. At control pH, I Ca, I K1, and I SS were not significantly different in Epi and Endo cells, but I K was larger in Epi cells. Acidosis did not alter I Ca, I K1, or I K but decreased I SS; this decrease was larger in Endo cells. It is suggested that the acidosis-induced decrease in I SS underlies the prolongation of the action potential. I Cl,ir at control pH was Cd2+ sensitive but 4,4′-disothiocyanato-stilbene-2,2′-disulfonic acid resistant. Acidosis increased I Cl,ir; it is suggested that the acidosis-induced increase in I Cl,ir underlies the depolarization of the resting membrane potential.

Oxygen- and temperature-dependent expression of survival protein kinases in crucian carp (Carassius carassius) heart and brain

2015 ◽  
Vol 308 (1) ◽  
pp. R50-R61 ◽  
Author(s):  
Göran E. Nilsson ◽  
Jarle Vaage ◽  
Kåre-Olav Stensløkken
Keyword(s):  
Protein Kinases ◽  
P38 Mapk ◽  
Crucian Carp ◽  
Oxygen Deprivation ◽  
Acclimation Temperature ◽  
Fresh Water Fish ◽  
Carassius Carassius ◽  
Cold Temperatures ◽  
Wide Range ◽  
Crucian Carp Carassius Carassius

Living without oxygen is limited to very few vertebrates, one species being the fresh water fish crucian carp ( Carassius carassius), which can survive months of anoxia at low temperatures. Mammalian heart and brain are particularly intolerant to oxygen deprivation, yet these organs can be conditioned to display increased resistance, possibly due to activation of several protein kinases. We hypothesized increased phosphorylation status of these kinases in hypoxic and anoxic crucian carp heart and brain. Moreover, we wanted to investigate whether the kinases showing the strongest phosphorylation during hypoxia/anoxia, ERK 1/2, p38-MAPK, JNK, PKCε, and PKCδ, also had increased expression and phosphorylation at cold temperatures, to better cope with the anoxic periods during winter. We found small differences in the phosphorylation status of ERK 1/2, p38-MAPK, JNK, PKCε, and PKCδ during 10 days of severe hypoxia in both heart and brain (0.3 mg O2/l) and varying responses to reoxygenation. In contrast, 7 days of anoxia (<0.01 mg O2/l) markedly increased phosphorylation of ERK 1/2, p38-MAPK, JNK in the heart, and p38-MAPK and PKCε in the brain. Similarly, varying acclimation temperature between 4, 10 and 20°C induced large changes in phosphorylation status. Total protein expression in heart and brain neither changed during different oxygen regimes nor with different acclimation temperatures, except for ERK 1/2, which slightly decreased in the heart at 4°C compared with 20°C. A phylogenetic analysis confirmed that these protein kinases are evolutionarily conserved across a wide range of vertebrate species. Our findings indicate important roles of several protein kinases during oxygen deprivation.

scholarly journals Cardiophysiological responses of the air-breathing Alaska blackfish to cold acclimation and chronic hypoxic submergence at 5°C

2020 ◽  
Vol 223 (22) ◽  
pp. jeb225730
Author(s):  
Jonathan A. W. Stecyk ◽  
Christine S. Couturier ◽  
Denis V. Abramochkin ◽  
Diarmid Hall ◽  
Asia Arrant-Howell ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cold Acclimation ◽  
Qt Interval ◽  
Gene Expression Pattern ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Active Lifestyle ◽  
Cold Temperatures ◽  
Contraction Coupling

ABSTRACTThe Alaska blackfish (Dallia pectoralis) remains active at cold temperatures when experiencing aquatic hypoxia without air access. To discern the cardiophysiological adjustments that permit this behaviour, we quantified the effect of acclimation from 15°C to 5°C in normoxia (15N and 5N fish), as well as chronic hypoxic submergence (6–8 weeks; ∼6.3–8.4 kPa; no air access) at 5°C (5H fish), on in vivo and spontaneous heart rate (fH), electrocardiogram, ventricular action potential (AP) shape and duration (APD), the background inward rectifier (IK1) and rapid delayed rectifier (IKr) K+ currents and ventricular gene expression of proteins involved in excitation–contraction coupling. In vivo fH was ∼50% slower in 5N than in 15N fish, but 5H fish did not display hypoxic bradycardia. Atypically, cold acclimation in normoxia did not induce shortening of APD or alter resting membrane potential. Rather, QT interval and APD were ∼2.6-fold longer in 5N than in 15N fish because outward IK1 and IKr were not upregulated in 5N fish. By contrast, chronic hypoxic submergence elicited a shortening of QT interval and APD, driven by an upregulation of IKr. The altered electrophysiology of 5H fish was accompanied by increased gene expression of kcnh6 (3.5-fold; Kv11.2 of IKr), kcnj12 (7.4-fold; Kir2.2 of IK1) and kcnj14 (2.9-fold; Kir2.4 of IK1). 5H fish also exhibited a unique gene expression pattern that suggests modification of ventricular Ca2+ cycling. Overall, the findings reveal that Alaska blackfish exposed to chronic hypoxic submergence prioritize the continuation of cardiac performance to support an active lifestyle over reducing cardiac ATP demand.

Changes in Immunological Parameters and Disease Resistance in Juvenile Coho Salmon (Oncorhynchus kisutch) in Response to Dehydroabietic Acid Exposure under Varying Thermal Conditions

2004 ◽  
Vol 39 (3) ◽  
pp. 175-182 ◽  
Author(s):  
Keith B. Tierney ◽  
Eric Stockner ◽  
Christopher J. Kennedy
Keyword(s):  
Coho Salmon ◽  
Thermal Conditions ◽  
Dehydroabietic Acid ◽  
Aeromonas Salmonicida ◽  
Acclimation Temperature ◽  
Dependent Manner ◽  
Immunological Parameters ◽  
Cold Temperatures ◽  
Temperature Shock ◽  
Exposure Temperature

Abstract This study explored the effects of a sublethal 96-h dehydroabietic acid (DHAA) exposure on aspects of the immune system of juvenile coho salmon under varying temperature conditions. Coho were exposed to DHAA concentrations below the determined LC50 value of 0.94 mg/L (95% confidence limits of 0.81 to 1.24 mg/L) for 96 h at either their acclimation temperature (8 or 18°C), or during an acute warm-shock (8 to 18°C) or cold-shock (18 to 8°C). Acclimation temperature alone significantly affected hematocrit (Hct), neutrophil respiratory burst activity (RBA) and leucocyte proportions. With temperature-shock, leucocrit (Lct), RBA and leucocyte proportions were altered. All parameters were affected by DHAA exposure, but not always in a dose-dependent manner. Across groups, DHAA caused Hct, lysozyme, thrombocyte, neutrophil and monocyte proportions to increase, and Lct, RBA and lymphocyte proportions to decrease. DHAA-temperature interactions resulted in the exacerbation of DHAA-induced effects. Exposure temperature had the most significant effect on the susceptibility of coho to Aeromonas salmonicida; fish were more susceptible at cold temperatures and when subjected to a temperature-shock compared to their respective controls. DHAA exposure modulated the response of temperature-shocked fish to this pathogen.

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