Alterations in electrical and contractile behavior of isolated cardiomyocytes by hydrogen peroxide: Possible ionic mechanisms

Beresewicz, A; Horackova, Magda

doi:10.1016/0022-2828(91)90133-7

Cited by 90 publications

(45 citation statements)

References 44 publications

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“…Therefore, an increase by H 2 O 2 of late I Na is expected to cause a significant prolongation of APD. Consistent with previous reports (Beresewicz and Horackova, 1991), we found that the early effect of H 2 O 2 on myocyte membrane potential was an increase in the duration of action potentials. This effect of H 2 O 2 can be largely explained by an increase of late I Na , because it was significantly attenuated by either ranolazine or TTX.…”

Section: Attenuation Of Arrhythmogenic Actions Of Ros 219supporting

confidence: 93%

Blocking Late Sodium Current Reduces Hydrogen Peroxide-Induced Arrhythmogenic Activity and Contractile Dysfunction

Song¹,

Shryock²,

Wagner³

et al. 2006

J Pharmacol Exp Ther

252

242

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Reactive oxygen species (ROS), including H 2 O 2 , cause intracellular calcium overload and ischemia-reperfusion damage. The objective of this study was to examine the hypothesis that H 2 O 2 -induced arrhythmic activity and contractile dysfunction are the results of an effect of H 2 O 2 to increase the magnitude of the late sodium current (late I Na ). Guinea pig and rabbit isolated ventricular myocytes were exposed to 200 M H 2 O 2 . Transmembrane voltages and currents and twitch shortening were measured using the whole-cell patch-clamp technique and video edge detection, respectively.

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Section: Attenuation Of Arrhythmogenic Actions Of Ros 219supporting

confidence: 93%

Blocking Late Sodium Current Reduces Hydrogen Peroxide-Induced Arrhythmogenic Activity and Contractile Dysfunction

Song¹,

Shryock²,

Wagner³

et al. 2006

J Pharmacol Exp Ther

252

242

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“…We and other groups have shown in guinea-pig and rat isolated myocytes that these changes are the consequence of intracellular calcium loading (Beresewicz & Horackova, 1991;Cerbai et al, 1991;Jabr & Cole, 1993;Mugelli et al, 1995), possibly involving abnormalities in sarcoplasmic reticulum Ca2+ release (Shattock et al, 1990;Boraso & Williams, 1994). In fact, prolongation of action potential duration and development of early-(EAD) and delayed afterdepolarizations (DAD) are prevented by intracellular EGTA (Cerbai et al, 1991;Jabr & Cole, 1993;Mugelli et al, 1995) and/or by pretreatment of the cells with ryanodine (Beresewics & Horachova, 1991).…”

Section: Introductionmentioning

confidence: 99%

The effect of oxygen free radicals on calcium current and dihydropyridine binding sites in guinea‐pig ventricular myocytes

Guerra

Cerbai

Gessi

et al. 1996

British J Pharmacology

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1 We used electrophysiological and binding techniques to determine the effects of oxygen free radicals (OFRs) generated by dihydroxyfumaric acid (DHF, 5 mM) on calcium current and dihydropyridine binding sites in guinea-pig isolated ventricular myocytes. 2 Binding of [3H]-PN200-110 to isolated ventricular myocytes revealed one population of binding sites with a KD of 0.11 + 0.01 nM and Bma, of 139.1 + 6.9 fmol mg' protein (n = 24). After 15 min of exposure to DHF, the density, but not the affinity of [3H]-PN200-110 binding sites was significantly (P<0.01) reduced to 35% of the control value (Bma,=49.4+ 3.7 fmol mg-' protein, KD= 0.11 + 0.01 nM, n= 15). 4 In myocytes incubated with the antilipoperoxidant agent, butylated hydroxytoluene (BHT, 50 uM), the decrease in [3H]-PN200-110 binding sites caused by DHF was partially prevented (Bmax values after 30 min exposure to DHF were 55.5+ 1.9 and 23.7 + 5.9 fmol mg-l protein in the presence and in the absence of BHT respectively, P<0.05). BHT did not affect the decrease in [3H]-PN200-110 binding sites during the first 15 min of exposure to DHF, but was able to prevent completely the further decrease occurring during the following 15 min of incubation with OFRs. 5 Our results demonstrate that the OFR-induced decrease in calcium current is associated with a reduction in DHP binding sites. The decrease in calcium current and in calcium channels may be implicated in the mechanical dysfunction associated with oxidative stress.

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“…Hayashi et al [44], Beresewicz et al [45], and Jabr and Cole [46] have reported that oxygen free radicals produced an initial prolongation of action potential duration of rat and guinea pig ventricular myocytes, and that the prolongation of action potential duration was followed by a shortening of duration. Pallandi et al [47] reported that xanthine oxidase-generated free radicals reduced the amplitude after 20 to 30 min exposure but did not affect the duration of the action potential in guinea pig ventricular strips.…”

Section: Ca 2 § Channelsmentioning

confidence: 99%

Oxygen free radicals and calcium homeostasis in the heart

et al. 1994

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Many experiments have been done to clarify the effects of oxygen free radicals on Ca 2+ homeostasis in the hearts. A burst of oxygen free radicals occurs immediately after reperfusion, but we have to be reminded that the exact levels of oxygen free radicals in the hearts are yet unknown in both physiological and pathophysiological conditions. Therefore, we should give careful consideration to this point when we perform the experiments and analyze the results.It is, however, evident that Ca 2+ overload occurs when the hearts are exposed to an excess amount of oxygen free radicals. Though ATP-independent Ca 2+ binding is increased, Ca 2+ influx through Ca 2 § channel does not increase in the presence of oxygen free radicals. Another possible pathway through which Ca 2. can enter the myocytes is Na+-Ca 2+ exchanger. Although, the activities ofNa § + ATPase and Na+-H + exchange are inhibited by oxygen free radicals, it is not known whether intracellular Na § level increases under oxidative stress or not. The question has to be solved for the understanding of the importance of Na § Ca z+ exchange in Ca 2+ influx process from extracellular space. Another question is 'which way does Na+-Ca 2+ exchange work under oxidative stress? Net influx or efflux of Ca 2 § ?' Membrane permeability for Ca 2+ may be maintained in a relatively early phase of free radical injury. Since sarcolemmal Ca2+-pumpATPase activity is depressed by oxygen free radicals, Ca 2 § extrusion from cytosol to extracellular space is considered to be reduced. It has also been shown that oxygen free radicals promote Ca 2 § release from sarcoplasmic reticulum and inhibit Ca 2+ sequestration to sarcoplasmic reticulum. Thus, these changes in Ca 2+ handling systems could cause the Ca 2+ overload due to oxygen free radicals. (Mol Cell Biochem 139: 91-100, 1994)

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Alterations in electrical and contractile behavior of isolated cardiomyocytes by hydrogen peroxide: Possible ionic mechanisms

Cited by 90 publications

References 44 publications

Blocking Late Sodium Current Reduces Hydrogen Peroxide-Induced Arrhythmogenic Activity and Contractile Dysfunction

Blocking Late Sodium Current Reduces Hydrogen Peroxide-Induced Arrhythmogenic Activity and Contractile Dysfunction

The effect of oxygen free radicals on calcium current and dihydropyridine binding sites in guinea‐pig ventricular myocytes

Oxygen free radicals and calcium homeostasis in the heart

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