Photoperiod-dependent modulation of cardiac excitation contraction coupling in the Siberian hamster

2005 ◽  
Vol 288 (3) ◽  
pp. R607-R614 ◽  
Author(s):  
K. M. Dibb ◽  
C. L. Hagarty ◽  
A. S. I. Loudon ◽  
A. W. Trafford
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Prolonged Exposure ◽  
Ventricular Myocytes ◽  
Short Photoperiod ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Excitation Contraction Coupling ◽  
Siberian Hamster ◽  
Contraction Coupling ◽  
Single Ventricular Myocytes ◽  
Cardiac Excitation

In mammals, changes in photoperiod regulate a diverse array of physiological and behavioral processes, an example of which in the Siberian hamster ( Phodopus sungorus) is the expression of bouts of daily torpor following prolonged exposure to a short photoperiod. During torpor, body temperature drops dramatically; however, unlike in nonhibernating or nontorpid species, the myocardium retains the ability to contract and is resistant to the development of arrhythmias. In the present study, we sought to determine whether exposure to a short photoperiod results in alterations to cardiac excitation-contraction coupling, thus potentially enabling the heart to survive periods of low temperature during torpor. Experiments were performed on single ventricular myocytes freshly isolated from the hearts of Siberian hamsters that had been exposed to either 12 wk of short-day lengths (SD) or 12 wk of long-day lengths (LD). In SD-acclimated animals, the amplitude of the systolic Ca2+ transient was increased (e.g., from 142 ± 17 nmol/l in LD to 229 ± 31 nmol/l in SD at 4 Hz; P < 0.001). The increased Ca2+ transient amplitude in the SD-acclimated animals was not associated with any change in the shape or duration of the action potential. However, sarcoplasmic reticulum Ca2+ content measured after current-clamp stimulation was increased in the SD-acclimated animals (at 4 Hz, 110 ± 5 vs. 141 ± 15 μmol/l, P < 0.05). We propose that short photoperiods reprogram the function of the cardiac sarcoplasmic reticulum, resulting in an increased Ca2+ content, and that this may be a necessary precursor for maintenance of cardiac function during winter torpor.

Differential Effects of Fentanyl and Morphine on Intracellular Ca2+Transients and Contraction in Rat Ventricular Myocytes 

1998 ◽  
Vol 89 (6) ◽  
pp. 1532-1542 ◽  
Author(s):  
Noriaki Kanaya ◽  
Daniel R. Zakhary ◽  
Paul A. Murray ◽  
Derek S. Damron
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Myocardial Contractility ◽  
Ventricular Myocytes ◽  
Free Acid ◽  
Intact Cells ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Rat Ventricular Myocytes ◽  
Fura 2 ◽  
Cardiac Excitation

Background Our objective was to elucidate the direct effects of fentanyl and morphine on cardiac excitation-contraction coupling using individual, field-stimulated rat ventricular myocytes. Methods Freshly isolated myocytes were loaded with fura-2 and field stimulated (0.3 Hz) at 28 degrees C. Amplitude and timing of intracellular Ca2+ concentration (at a 340:380 ratio) and myocyte shortening (video edge detection) were monitored simultaneously in individual cells. Real time Ca2+ uptake into isolated sarcoplasmic reticulum vesicles was measured using fura-2 free acid in the extravesicular compartment. Results The authors studied 120 cells from 30 rat hearts. Fentanyl (30-1,000 nM) caused dose-dependent decreases in peak intracellular Ca2+ concentration and shortening, whereas morphine (3-100 microM) decreased shortening without a concomitant decrease in the Ca2+ transient. Fentanyl prolonged the time to peak and to 50% recovery for shortening and the Ca2+ transient, whereas morphine only prolonged the timing parameters for shortening. Morphine (100 microM), but not fentanyl (1 microM), decreased the amount of Ca2+ released from intracellular stores in response to caffeine in intact cells, and it inhibited the rate of Ca2+ uptake in isolated sarcoplasmic reticulum vesicles. Fentanyl and morphine both caused a downward shift in the dose-response curve to extracellular Ca2+ for shortening, with no concomitant effect on the Ca2+ transient. Conclusions Fentanyl and morphine directly depress cardiac excitation-contraction coupling at the cellular level. Fentanyl depresses myocardial contractility by decreasing the availability of intracellular Ca2+ and myofilament Ca2+ sensitivity. In contrast, morphine depresses myocardial contractility primarily by decreasing myofilament Ca2+ sensitivity.

Overexpression of human β2-adrenergic receptors increases gain of excitation-contraction coupling in mouse ventricular myocytes

2004 ◽  
Vol 287 (3) ◽  
pp. H1029-H1038 ◽  
Author(s):  
Scott A. Grandy ◽  
Eileen M. Denovan-Wright ◽  
Gregory R. Ferrier ◽  
Susan E. Howlett
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Adrenergic Receptors ◽  
Action Potentials ◽  
Ventricular Myocytes ◽  
Wild Type ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Cardiac Excitation ◽  
Action Potential Configuration

This study investigated cardiac excitation-contraction coupling at 37°C in transgenic mice with cardiac-specific overexpression of human β2-adrenergic receptors (TG4 mice). In field-stimulated myocytes, contraction was significantly greater in TG4 compared with wild-type (WT) ventricular myocytes. In contrast, when duration of depolarization was controlled with rectangular voltage clamp steps, contraction amplitudes initiated by test steps were the same in WT and TG4 myocytes. When cells were voltage clamped with action potentials simulating TG4 and WT action potential configurations, contractions were greater with long TG4 action potentials and smaller with shorter WT action potentials, which suggests an important role for action potential configuration. Interestingly, peak amplitude of L-type Ca2+ current ( ICa-L) initiated by rectangular test steps was reduced, although the voltage dependencies of contractions and currents were not altered. To explore the basis for the altered relation between contraction and ICa-L, Ca2+ concentrations were measured in myocytes loaded with fura 2. Diastolic concentrations of free Ca2+ and amplitudes of Ca2+ transients were similar in voltage-clamped myocytes from WT and TG4 mice. However, sarcoplasmic reticulum (SR) Ca2+ content assessed with the rapid application of caffeine was elevated in TG4 cells. Increased SR Ca2+ was accompanied by increased frequency and amplitudes of spontaneous Ca2+ sparks measured at 37°C with fluo 3. These observations suggest that the gain of Ca2+-induced Ca2+ release is increased in TG4 myocytes. Increased gain counteracts the effects of decreased amplitude of ICa-L in voltage-clamped myocytes and likely contributes to increased contraction amplitudes in field-stimulated TG4 myocytes.

Thiopental Alters Contraction, Intracellular Ca2+, and pH in Rat Ventricular Myocytes 

1998 ◽  
Vol 89 (1) ◽  
pp. 202-214 ◽  
Author(s):  
Noriaki Kanaya ◽  
Daniel R. Zakhary ◽  
Paul A. Murray ◽  
Derek S. Damron
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Intracellular Ph ◽  
Ventricular Myocytes ◽  
Negative Inotropic Effect ◽  
Inotropic Effect ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Rat Ventricular Myocytes ◽  
Fura 2 ◽  
Cardiac Excitation

Background Myocardial contractility is regulated by intracellular concentration of free Ca2+ ([Ca2'],) and myofilament Ca2+ sensitivity. The objective of this study was to elucidate the direct effects of thiopental on cardiac excitation-contraction coupling using individual, field-stimulated ventricular myocytes. Methods Freshly isolated rat ventricular myocytes were loaded with the Ca2+ indicator, fura-2, and placed on the stage of an inverted fluorescence microscope in a temperature-regulated bath. [Ca2+], (340/380 ratio) and myocyte shortening (video-edge detection) were monitored simultaneously in individual cells field-stimulated at 0.3 Hz. Amplitude and timing of myocyte shortening and [Ca2+l, were compared before and after addition of thiopental. Intracellular pH was measured with the pH indicator, BCECF (500/440 ratio). Real-time uptake of Ca2+ into isolated sarcoplasmic reticulum vesicles was measured using fura-2 free acid in the extravesicular compartment. One hundred thirty-two cells were studied. Results Field stimulation increased [Ca2+]i from 85 + 10 nM to 355 + 22 nM (mean + SEM). Myocytes shortened by 10% of resting cell length (127 + 5 tlm). Times to peak [Ca2+], and shortening were 139 + 6 and 173 + 7 msec, respectively. Times to 50% recovery for [Ca2+], and shortening were 296 + 6 and 290 + 6 ms, respectively. Addition of thiopental (30-1,000 /lM) resulted in dose-dependent decreases in peak [Ca2+]i and myocyte shortening. Thiopental altered time to peak and time to 50% recovery for [Ca2+], and myocyte shortening and inhibited the rate of uptake of Ca2+ into isolated sarcoplasmic reticulum vesicles. Thiopental did not, however, alter the amount of Ca2+ released in response to caffeine in sarcoplasmic reticulum vesicles or intact cells. Thiopental (100 uM) increased intracellular pH and caused an upward shift in the dose-response curve to extracellular Ca2+ for shortening, with no concomitant effect on peak [Ca2+],. These effects were abolished by ethylisopropyl amiloride, an inhibitor of Na+-H+ exchange. Conclusion Thiopental has a direct negative inotropic effect on cardiac excitation-contraction coupling at the cellular level, which is mediated by a decrease in [Ca2+],. Thiopental also increases myofilament Ca2+ sensitivity via alkalinization of the cell, which may partially offset its negative inotropic effect.

scholarly journals Models of cardiac excitation–contraction coupling in ventricular myocytes

2010 ◽  
Vol 226 (1) ◽  
pp. 1-15 ◽  
Author(s):  
George S.B. Williams ◽  
Gregory D. Smith ◽  
Eric A. Sobie ◽  
M. Saleet Jafri
Keyword(s):  
Ventricular Myocytes ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Cardiac Excitation

scholarly journals The recombinant dihydropyridine receptor II–III loop and partly structured ‘C’ region peptides modify cardiac ryanodine receptor activity

2005 ◽  
Vol 385 (3) ◽  
pp. 803-813 ◽  
Author(s):  
Angela F. DULHUNTY ◽  
Yamuna KARUNASEKARA ◽  
Suzanne M. CURTIS ◽  
Peta J. HARVEY ◽  
Philip G. BOARD ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Secondary Structure ◽  
Cardiac Muscle ◽  
Ryanodine Receptor ◽  
Structure Analysis ◽  
Room Temperature ◽  
Random Coil ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling

A physical association between the II–III loop of the DHPR (dihydropryidine receptor) and the RyR (ryanodine receptor) is essential for excitation–contraction coupling in skeletal, but not cardiac, muscle. However, peptides corresponding to a part of the II–III loop interact with the cardiac RyR2 suggesting the possibility of a physical coupling between the proteins. Whether the full II–III loop and its functionally important ‘C’ region (cardiac DHPR residues 855–891 or skeletal 724–760) interact with cardiac RyR2 is not known and is examined in the present study. Both the cardiac DHPR II–III loop (CDCL) and cardiac peptide (Cc) activated RyR2 channels at concentrations >10 nM. The skeletal DHPR II–III loop (SDCL) activated channels at ≤100 nM and weakly inhibited at ≥1 μM. In contrast, skeletal peptide (Cs) inhibited channels at all concentrations when added alone, or was ineffective if added in the presence of Cc. Ca2+-induced Ca2+ release from cardiac sarcoplasmic reticulum was enhanced by CDCL, SDCL and the C peptides. The results indicate that the interaction between the II–III loop and RyR2 depends critically on the ‘A’ region (skeletal DHPR residues 671–690 or cardiac 793–812) and also involves the C region. Structure analysis indicated that (i) both Cs and Cc are random coil at room temperature, but, at 5 °C, have partial helical regions in their N-terminal and central parts, and (ii) secondary-structure profiles for CDCL and SDCL are similar. The data provide novel evidence that the DHPR II–III loop and its C region interact with cardiac RyR2, and that the ability to interact is not isoform-specific.

scholarly journals Ca2+ cycling in cardiomyocytes from a high-performance reptile, the varanid lizard (Varanus exanthematicus)

2009 ◽  
Vol 297 (6) ◽  
pp. R1636-R1644 ◽  
Author(s):  
Gina L. J. Galli ◽  
Daniel E. Warren ◽  
Holly A. Shiels
Keyword(s):  
Sarcoplasmic Reticulum ◽  
High Performance ◽  
Time Course ◽  
Ventricular Myocytes ◽  
Volume Ratio ◽  
Voltage Sensitivity ◽  
Excitation Contraction Coupling ◽  
Electrophysiological Properties ◽  
Contraction Coupling ◽  
Cardiovascular Performance

The varanid lizard possesses one of the largest aerobic capacities among reptiles with maximum rates of oxygen consumption that are twice that of other lizards of comparable sizes at the same temperature. To support this aerobic capacity, the varanid heart possesses morphological adaptations that allow the generation of high heart rates and blood pressures. Specializations in excitation-contraction coupling may also contribute to the varanids superior cardiovascular performance. Therefore, we investigated the electrophysiological properties of the l-type Ca2+ channel and the Na+/Ca2+ exchanger (NCX) and the contribution of the sarcoplasmic reticulum to the intracellular Ca2+ transient (Δ[Ca2+]i) in varanid lizard ventricular myocytes. Additionally, we used confocal microscopy to visualize myocytes and make morphological measurements. Lizard ventricular myocytes were found to be spindle-shaped, lack T-tubules, and were ∼190 μm in length and 5–7 μm in width and depth. Cardiomyocytes had a small cell volume (∼2 pL), leading to a large surface area-to-volume ratio (18.5), typical of ectothermic vertebrates. The voltage sensitivity of the l-type Ca2+ channel current ( ICa), steady-state activation and inactivation curves, and the time taken for recovery from inactivation were also similar to those measured in other reptiles and teleosts. However, transsarcolemmal Ca2+ influx via reverse mode Na+/Ca2+ exchange current was fourfold higher than most other ectotherms. Moreover, pharmacological inhibition of the sarcoplasmic reticulum led to a 40% reduction in the Δ[Ca2+]i amplitude, and slowed the time course of decay. In aggregate, our results suggest varanids have an enhanced capacity to transport Ca2+ through the Na+/Ca2+ exchanger, and sarcoplasmic reticulum suggesting specializations in excitation-contraction coupling may provide a means to support high cardiovascular performance.

Excitation–contraction coupling in isolated adult ventricular myocytes from the rat, dog, and rabbit: effects of various inotropic interventions in the presence of ryanodine

1986 ◽  
Vol 64 (12) ◽  
pp. 1473-1483 ◽  
Author(s):  
Magda Horackova
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ventricular Myocytes ◽  
Inotropic Agents ◽  
Inhibitory Effects ◽  
Pharmacological Interventions ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Ventricular Cells ◽  
Contractile Activation ◽  
Dog Myocytes

Enzymatically isolated ventricular cells from rats, dogs, and rabbits were electrically stimulated and their membrane potentials were recorded simultaneously with their contractions. Specific pharmacological interventions were used to assess the relative roles of transsarcolemmal Ca2+ entry and the Ca2+ release by the sarcoplasmic reticulum in activating contractions, in these myocytes. We used ryanodine and caffeine to influence Ca2+ release by the sarcoplasmic reticulum, BAY K 8644 and epinephrine to increase Ca2+ entry through Ca2+ channels, and veratridine, ouabain, and monensin to increase Ca2+ entry through Na+–Ca2+ exchange. Ryanodine (1 μM) completely inhibited the shortenings in rat and dog myocytes, but the contractions in rabbit myocytes were much less sensitive to this alkaloid. Similar inhibitory effects of ryanodine were observed in the presence of various inotropic agents with two exceptions: caffeine's effect on the dog myocytes was relatively insensitive to ryanodine and the long-lasting tonic contractions that veratridine triggered in the myocytes of all three species remained completely unaffected by ryanodine. The data indicate that contractile activation in rat and dog ventricular cells is strongly dependent on Ca2+ release from the sarcoplasmic reticulum, while contractility in rabbit myocytes seems to be more dependent on Ca2+ entry through the sarcolemma. The ryanodine-resistant tonic contractions triggered in the myocytes of all three species in the presence of veratridine may be activated by an increased Ca2+ entry via Na+–Ca2+ exchange.

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.

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