scholarly journals Sulfur Dioxide Derivative Prevents the Prolongation of Action Potential During the Isoproterenol-Induced Hypertrophy of Rat Cardiomyocytes

2021 ◽  
Vol 93 (suppl 3) ◽  
Author(s):  
UĞUR DALAMAN ◽  
HASAN ÖZDOĞAN ◽  
AHMED K. SIRCAN ◽  
SEVGI A. ŞENGÜL ◽  
NAZMI YARAŞ
2001 ◽  
Vol 90 (5) ◽  
pp. 1720-1728 ◽  
Author(s):  
Xue-Qian Zhang ◽  
Lian-Qin Zhang ◽  
Bradley M. Palmer ◽  
Yuk-Chow Ng ◽  
Timothy I. Musch ◽  
...  

Two electrophysiological manifestations of myocardial infarction (MI)-induced myocyte hypertrophy are prolongation of action potential duration (APD) and reduction of transient outward current ( I to) density. Because high-intensity sprint training (HIST) ameliorated myocyte hypertrophy and improved myocyte Ca2+ homeostasis and contractility after MI, the present study evaluated whether 6–8 wk of HIST would shorten the prolonged APD and improve the depressed I to in post-MI myocytes. There were no differences in resting membrane potential and action potential amplitude (APA) measured in myocytes isolated from sham-sedentary (Sed), MI-Sed, and MI-HIST groups. Times required for repolarization to 50 and 90% APA were significantly ( P < 0.001) prolonged in MI-Sed myocytes. HIST reduced times required for repolarization to 50 and 90% APA to values observed in Sham-Sed myocytes. The fast and slow components of I towere significantly ( P < 0.0001) reduced in MI-Sed myocytes. HIST significantly ( P < 0.001) enhanced the fast and slow components of I to in MI myocytes, although not to levels observed in Sham-Sed myocytes. There were no significant differences in steady-state I toinactivation and activation parameters among Sham-Sed, MI-Sed, and MI-HIST myocytes. Likewise, recovery from time-dependent inactivation was also similar among the three groups. We suggest that normalization of APD after MI by HIST may be mediated by restoration of I to toward normal levels.


1996 ◽  
Vol 1 (3) ◽  
pp. 229-234 ◽  
Author(s):  
Regan T. Pallandi ◽  
Nigel H. Lovell ◽  
Terence J. Campbell

Background Dofetilide is a new class III antiarrhythmic agent with demonstrated efficacy in ventricular and atrial tachyarrhythmias. We investigated its class HI actions and their modulation by stimulation rate in rabbit atrial myocardium. Methods and Results Standard microelectrode techniques were used to record action potentials from rabbit atrial tissue at varying stimulation rates. Dofetilide produced a dose-dependent prolongation of action potential duration at concentrations from 1 nM to 1 μM at an interstimulus interval of 1000 ms. Action potential duration at 90% repolarization (action potential duration) was prolonged from 116 ± 11.7 ms in control solutions to 148 ± 13.9 ms at 1nM dofetilide and 186 ± 49.3 ms at 1 μM dofetilide ( P < .05 for 1 nM vs control; P < .01 for 1 μM vs control). Reduction of interstimulus interval to 500 ms had no significant effect on action potential duration prolongation by dofetilide. At faster rates than this, and particularly at an interstimulus interval less than 330 ms, a marked “reverse rate dependence” of the class III effect was observed. Specifically, the high therapeutic concentration of 10 nM showed no effect on action potential duration at interstimulus interval of 250 ms or 200 ms, and even at a concentration of 30 nM, the small class III effect was no longer statistically significant at these rates. Conclusion Dofetilide prolongs action potential duration in rabbit atrial myocardium, but this effect is significantly attenuated at stimulation rates above 2 Hz.


2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
M. Pásek ◽  
J. Šimurda ◽  
G. Christé

The ratio of densities of Na-Ca exchanger current (INaCa) in the t-tubular and surface membranes (INaCa-ratio) computed from the values ofINaCaand membrane capacitances (Cm) measured in adult rat ventricular cardiomyocytes before and after detubulation ranges between 1.7 and 25 (potentially even 40). Variations of action potential waveform and of calcium turnover within this span of theINaCa-ratio were simulated employing previously developed model of rat ventricular cell incorporating separate description of ion transport systems in the t-tubular and surface membranes. The increase ofINaCa-ratio from 1.7 to 25 caused a prolongation of APD (duration of action potential at 90% repolarisation) by 12, 9, and 6% and an increase of peak intracellular Ca2+transient by 45, 19, and 6% at 0.1, 1, and 5 Hz, respectively. The prolonged APD resulted from the increase ofINaCadue to the exposure of a larger fraction of Na-Ca exchangers to higher Ca2+transients under the t-tubular membrane. The accompanying rise of Ca2+transient was a consequence of a higher Ca2+load in sarcoplasmic reticulum induced by the increased Ca2+cycling between the surface and t-tubular membranes. However, the reason for large differences in theINaCa-ratio assessed from measurements in adult rat cardiomyocytes remains to be explained.


1996 ◽  
Vol 27 (2) ◽  
pp. 374-375
Author(s):  
Jügen Schreieck ◽  
Viktor Gjini ◽  
Michael Korth ◽  
Albert Schömig ◽  
Claus Schmitt

2006 ◽  
Vol 345 (3) ◽  
pp. 1116-1121 ◽  
Author(s):  
Yasutaka Tanabe ◽  
Katsuharu Hatada ◽  
Naoki Naito ◽  
Yoshiyasu Aizawa ◽  
Masaomi Chinushi ◽  
...  

Heart Rhythm ◽  
2005 ◽  
Vol 2 (8) ◽  
pp. 860-866 ◽  
Author(s):  
Jiqing Guo ◽  
Shu Zhan ◽  
James P. Lees-Miller ◽  
GuoQi Teng ◽  
Henry J. Duff

1992 ◽  
Vol 263 (5) ◽  
pp. C953-C958 ◽  
Author(s):  
S. Sunano ◽  
K. Moriyama ◽  
K. Shimamura

The effect of sodium vanadate on action potential and twitch contraction of guinea pig ureter was studied and compared with that of ouabain, elevated K+, low temperature, and a Ca agonist (BAY K 8644), which can be expected to exert certain comparative effects. Sodium vanadate markedly potentiated twitch contraction. Potentiation by vanadate was associated with marked prolongation of relaxation time. Sodium vanadate caused only slight depolarization of the membrane but marked changes in action potential. The duration of action potential was prolonged and the number of oscillatory spike potentials increased. These effects were different from those of other treatments. It is concluded that prolongation of action potential and the increase in the number of spikes are the main cause of potentiation of twitch contraction by sodium vanadate. In addition, inhibition of Ca pump activity of the smooth muscle membrane system by vanadate might also be involved in potentiation of twitch contraction.


2006 ◽  
Vol 50 (5) ◽  
pp. 557
Author(s):  
Sun Jun Bae ◽  
Myung Hee Kim ◽  
Jee Eun Chae ◽  
Chong Hoon Kim ◽  
Kyung Tae Min ◽  
...  

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