scholarly journals The arrhythmogenic transient inward current iTI and related contraction in isolated guinea-pig ventricular myocytes.

1987 ◽  
Vol 392 (1) ◽  
pp. 523-542 ◽  
Author(s):  
D Fedida ◽  
D Noble ◽  
A C Rankin ◽  
A J Spindler
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Inward Current ◽  
Transient Inward Current

Caffeine-induced Ca2+ release activates Ca2+ extrusion via Na+-Ca2+ exchanger in cardiac myocytes

1989 ◽  
Vol 257 (1) ◽  
pp. C147-C152 ◽  
Author(s):  
G. Callewaert ◽  
L. Cleemann ◽  
M. Morad
Keyword(s):  
Guinea Pig ◽  
Cardiac Myocytes ◽  
Time Course ◽  
Ventricular Myocytes ◽  
Whole Cell ◽  
Inward Current ◽  
Fura 2 ◽  
Transient Inward Current ◽  
Inward Currents

Rapid application of caffeine in fura-2-dialyzed and whole cell-clamped rat and guinea pig ventricular myocytes activated reversibly large intracellular Ca2+ transients that accompanied Na+-dependent transient inward currents. Such transient inward currents had the same time course as the intracellular Ca2+ transient and were suppressed by Ni2+ and removal of extracellular Na+. Because Ca2+ release signals were not altered by addition of Ni2+ or removal of Na+, we concluded that the rise in intracellular Ca2+ concentration was necessary for the activation of the transient inward current. Thus the caffeine-induced transient inward current represents efflux of Ca2+ via the Na+-Ca2+ exchanger.

Electroporation-Induced Inward Current in Voltage-Clamped Guinea Pig Ventricular Myocytes

2010 ◽  
Vol 238 (1-3) ◽  
pp. 69-80 ◽  
Author(s):  
Oksana Dyachok ◽  
Pavel Zhabyeyev ◽  
Terence F. McDonald
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Inward Current

Abstract 17193: Inhibiting Late Sodium Current Attenuates Isoproterenol-Induced Transient Inward Current and Delayed Afterdepolarizations in Ventricular Myocytes

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Yejia Song ◽  
Nesrine El-Bizri ◽  
Sridharan Rajamani ◽  
Luiz Belardinelli
Keyword(s):  
Ventricular Myocytes ◽  
Sodium Current ◽  
Selective Inhibition ◽  
Adrenergic Stimulation ◽  
Patch Clamp Technique ◽  
Cardiac Tissues ◽  
Inward Current ◽  
Transient Inward Current ◽  
Whole Cell Patch Clamp ◽  
Series Of Experiments

Introduction: The β-adrenergic agonist isoproterenol (ISO) is known to induce the arrhythmogenic transient inward current (I Ti ) and delayed afterdepolarization (DAD) via a stimulation of L-type Ca 2+ current. Recent studies found that ISO-induced DADs in cardiac tissues are inhibited by GS967, a selective blocker of the late Na + current (I NaL ). Thus, we hypothesize that I NaL contributes to the actions of ISO, and selective inhibition of this current will reduce ISO-induced I Ti and DADs. Methods: Transmembrane currents and action potentials of rabbit and guinea pig (GP) ventricular myocytes were recorded using the whole-cell patch-clamp technique. ISO (0.1 μM), GS967 (1 μM) and the Na + channel blocker tetrodotoxin (TTX, 3 μM) were used in the experiments. Results: In rabbit myocytes, application of ISO caused an increase in the amplitude of I NaL from -0.10±0.03 to -0.32±0.04 pA/pF (n = 17, p < 0.05). The ISO-stimulated I NaL was inhibited by GS967 and TTX. In one series of experiments, ISO increased the I NaL from -0.14±0.04 to -0.35±0.06 pA/pF, and GS967 applied in the presence of ISO reduced the current to -0.14±0.03 pA/pF (n = 9, p < 0.05). In another series of experiments, the amplitude of I NaL was increased by ISO from -0.17±0.08 to -0.41±0.09 pA/pF, and was decreased to -0.09±0.08 pA/pF when TTX was applied with ISO (n = 5, p < 0.05). Application of ISO also induced I Ti and DADs. GS967 applied in the presence of ISO inhibited the amplitude of I Ti by 52±6%, from -1.79±0.30 to -0.87±0.16 pA/pF (n = 8, p < 0.05). Consistent with the inhibition of I Ti , GS967 suppressed the amplitude of ISO-induced DADs by 56±12%, from 6.54±1.59 to 3.22±1.27 mV (n = 5, p < 0.05). Similarly, in GP myocytes ISO-induced I Ti and DADs were decreased by GS967 from -1.14±0.21 to -0.73±0.16 pA/pF (n = 7, p < 0.05) and from 7.16±0.59 to 4.67±0.24 mV (n = 5, p < 0.05), respectively. Conclusions: An increased I NaL is likely to contribute to the proarrhythmic effects of ISO in cardiac myocytes. GS967 significantly attenuated ISO-induced I NaL , I Ti and DADs, suggesting that inhibiting this current could be an effective strategy to antagonize the arrhythmogenic actions of β-adrenergic stimulation.

scholarly journals Inward current related to contraction in guinea-pig ventricular myocytes.

1987 ◽  
Vol 385 (1) ◽  
pp. 565-589 ◽  
Author(s):  
D Fedida ◽  
D Noble ◽  
Y Shimoni ◽  
A J Spindler
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Inward Current

Palmitoylcarnitine increases [Na+]i and initiates transient inward current in adult ventricular myocytes

1995 ◽  
Vol 268 (6) ◽  
pp. H2405-H2417 ◽  
Author(s):  
J. Wu ◽  
P. B. Corr
Keyword(s):  
Ventricular Myocytes ◽  
Cell Voltage ◽  
Adult Rabbit ◽  
Inward Current ◽  
Transient Inward Current ◽  
Delayed Afterdepolarizations ◽  
Rabbit Ventricular Myocytes ◽  
The Relationship ◽  
Sensitive Electrode ◽  
Modest Effect

This study was performed to determine whether long-chain acylcarnitines, specifically palmitoylcarnitine, could account for the increase in intracellular Na+ ([Na+]i) during ischemia eliciting a secondary increase in intracellular Ca2+ ([Ca2+]i). Accordingly, whole cell voltage-clamp procedures and Na(+)-sensitive electrode recordings were employed simultaneously in isolated adult rabbit ventricular myocytes to assess the relationship between activation of a slow-inactivating Na+ current [INa(s)] and a potential increase in [Na+]i. The [Na+]i increased progressively from 8.4 +/- 1.2 to 22.5 +/- 1.8 mM (n = 8, P < 0.01) on exposure to palmitoylcarnitine (10 microM) accompanied by the activation of INa(s); both effects were reversible. Inhibition of INa(s) by tetrodotoxin (TTX, 10 microM) inhibited the increase in [Na+]i. Increasing [Na+]i to 20 mM without ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) to mimic effects measured with palmitoylcarnitine consistently elicited the transient inward current (Iti) and delayed afterdepolarizations (DADs). The percent inhibition (12.9 +/- 2.8%) of the Na(+)-K(+)-adenosinetriphosphatase pump activity by palmitoylcarnitine (10 microM) was much smaller than that induced by ouabain (10 microM, 90.5 +/- 2.5%), suggesting that this modest effect of palmitoylcarnitine on the pump is unlikely to account for the increase in [Na+]i induced by palmitoylcarnitine. Thus palmitoylcarnitine induces the INa(s) leading to an increase in [Na+]i, which elicits an increase in [Ca2+]i probably via the Na+/Ca2+ exchanger, thereby leading to the development of Iti and DADs.

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