Effects of the blockade of cardiac sarcolemmal ATP-sensitive potassium channels on arrhythmias and coronary flow in ischemia–reperfusion model in isolated rat hearts

Gök, Şule; Vural, Kamıl; Seküri, Cevad; Onur, Rüştü; Tezcan, Alp; İzanlı, Ahenk

doi:10.1016/j.vph.2005.11.006

Cited by 15 publications

(7 citation statements)

References 40 publications

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“…28 In a recent study, HMR 1098 was shown to reduce the number of premature ventricular beats, but it did not decrease the incidence of reperfusion-induced VF in isolated rat hearts. 29 In the current study, a 3-mg/kg dose of HMR 1098 was used and found to decrease the duration of ventricular arrhythmia during I/R in anesthetized rats. To our knowledge, this is the first report of the effect of HMR 1098 on reperfusioninduced arrhythmias in anesthetized rats.…”

Section: The Effect Of K Atp Modulators On I/r-induced Arrhythmias Inmentioning

confidence: 95%

Both Mitochondrial KATP Channel Opening and Sarcolemmal KATP Channel Blockage Confer Protection Against Ischemia/Reperfusion-Induced Arrhythmia in Anesthetized Male Rats

Gonca

Bozdoğan

2010

J Cardiovasc Pharmacol Ther

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results of the current study indicate that both mitochondrial K(ATP) channel activation and sarcolemmal K(ATP) channel inhibition exert antiarrhythmic action in male rats. The antiarrhythmic effect of pinacidil is not depend on the sarcolemmal K(ATP) channel opening. These results also indicate that K(ATP) channel modulators show no discernable effect in female rats due to the already low incidence of arrhythmias in females.

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Section: The Effect Of K Atp Modulators On I/r-induced Arrhythmias Inmentioning

confidence: 95%

Both Mitochondrial KATP Channel Opening and Sarcolemmal KATP Channel Blockage Confer Protection Against Ischemia/Reperfusion-Induced Arrhythmia in Anesthetized Male Rats

Gonca

Bozdoğan

2010

J Cardiovasc Pharmacol Ther

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“…Although the contribution of mito‐ and/or sarc‐K ATP to this phenomenon is still the object of intense debate, [32] a prevalent role of mito‐K ATP in reducing the cell apoptotic death following ischaemia/reperfusion is suggested by several studies; [33,34] indeed, selective openers of mito‐K ATP are viewed as promising anti‐ischaemic drugs [35–38] . Nevertheless, there is also clear evidence about the possible contribution of sarc‐K ATP in reducing the ischaemia‐induced injury and, in particular, the arrhythmias associated with ischaemia/reperfusion [39–41] …”

Section: Discussionmentioning

confidence: 99%

Effects of K_ATPopeners on the QT prolongation induced by HERG-blocking drugs in guinea-pigs

Testai¹,

Cecchetti²,

Sabatini³

et al. 2010

Journal of Pharmacy and Pharmacology

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Objectives This work evaluated the potential usefulness of pharmacological activation of cardiac ATP-sensitive potassium channels (KATP) in the prevention of drug-induced QT prolongation in anaesthetised guinea-pigs. Prolongation of cardiac repolarisation and QT interval is an adverse effect of many drugs blocking HERG potassium channels. This alteration can be dangerously arrhythmogenic and has been associated with the development of a particular form of ventricular tachyarrhythmia known as torsade de pointes. Methods The well-known KATP openers aprikalim, cromakalim and pinacidil were used. Moreover, three benzothiazine derivatives, which have been reported as potent activators of KATP channels, were also used. Key findings Pharmacological activation of KATP channels caused a reduction of the QT prolongation, induced by astemizole, cisapride, quinidine and thioridazine. In contrast, the QT prolongation induced by haloperidol, sotalol and terfenadine, which are known to block HERG channels but also KATP channels, was not influenced by KATP activation. Glibenclamide and tolbutamide (non-selective blockers of KATP channels expressed both in sarcolemmal and in mitochondrial membranes) antagonised the effects of KATP openers, whereas 5-hydroxydecanoic acid (selective blocker of the mitochondrial KATP channels) failed to antagonise the effects of KATP openers, indicating that only the sarcolemmal KATP is involved in the cardioprotective activity. Conclusions The data suggest that pharmacological KATP activation might represent an option for treatment of patients exposed to QT-prolonging drugs.

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“…The cell with stripes were chosen in the experimental process because their surface is smooth, short, columnar, and stationary. Calcium-tolerant ventricular myocytes were easily selected (Gok et al, 2006;Gumina et al, 2007).…”

Section: Cell Isolationmentioning

confidence: 99%

Effect of pinacidil on rat ventricular myocytes during transient hypoxia and reperfusion

Dong

Zhu

2014

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to evaluate the cardioprotective effect of pinacidil postconditioning on rat hearts with transient hypoxia and reperfusion. An acute myocardial anoxia-reperfusion rat model was created by ligating coronary arteries for 10 min and subsequent reperfusion for 60 min. Twenty-four rats in 4 groups received different treatments: normal hearts as control (N = 6), anoxia-reperfusion (A/R) only (N = 6), pinacidil postconditioning (N = 6), and pinacidil plus adenosine triphosphate-sensitive potassium channel inhibitors (glibenclamide) (N = 6). The kinetic parameters and electrophysiological properties, including early apoptosis protein expression changes of Bax, Bcl-2, and FN were examined using the isolated perfusion and patch-clamp technique and immunohistochemistry. The left ventricular systolic pressure and maximum -dp/dt in A/R groups were significantly higher than those in the control group (P < 0.05). The left ventricular developing pressure, maximum +dp/dt, and heart rate in the A/R group were slightly decreased. The pinacidil-postconditioned group has better cardiac function recovery after ischemia/reperfusion than the A/R group (P < 0.01). In addition, using the patch-clamp technique, the mean open time and conductance values are significantly higher in the pinacidil postconditioning group, compared with those in the A/R group. The FN) increased during A/R, while Bcl-2 protein expression decreased. A significant difference was found in the pinacidil treatment group relative to the A/R group. Pinacidil postconditioning can exert cardioprotective effects on A/R-injured rat hearts, which may indicate a potential application of pinacidil postconditioning to protect A/R-injured hearts.

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Effects of the blockade of cardiac sarcolemmal ATP-sensitive potassium channels on arrhythmias and coronary flow in ischemia–reperfusion model in isolated rat hearts

Cited by 15 publications

References 40 publications

Both Mitochondrial KATP Channel Opening and Sarcolemmal KATP Channel Blockage Confer Protection Against Ischemia/Reperfusion-Induced Arrhythmia in Anesthetized Male Rats

Both Mitochondrial KATP Channel Opening and Sarcolemmal KATP Channel Blockage Confer Protection Against Ischemia/Reperfusion-Induced Arrhythmia in Anesthetized Male Rats

Effects of K_ATPopeners on the QT prolongation induced by HERG-blocking drugs in guinea-pigs

Effect of pinacidil on rat ventricular myocytes during transient hypoxia and reperfusion

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Effects of the blockade of cardiac sarcolemmal ATP-sensitive potassium channels on arrhythmias and coronary flow in ischemia–reperfusion model in isolated rat hearts

Cited by 15 publications

References 40 publications

Both Mitochondrial KATP Channel Opening and Sarcolemmal KATP Channel Blockage Confer Protection Against Ischemia/Reperfusion-Induced Arrhythmia in Anesthetized Male Rats

Both Mitochondrial KATP Channel Opening and Sarcolemmal KATP Channel Blockage Confer Protection Against Ischemia/Reperfusion-Induced Arrhythmia in Anesthetized Male Rats

Effects of KATPopeners on the QT prolongation induced by HERG-blocking drugs in guinea-pigs

Effect of pinacidil on rat ventricular myocytes during transient hypoxia and reperfusion

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Effects of K_ATPopeners on the QT prolongation induced by HERG-blocking drugs in guinea-pigs