Blockade by antiarrhythmic drugs of glibenclamide‐sensitive K<sup>+</sup> channels in <i>Xenopus</i> oocytes

Sakuta, Hidenari; Okamoto, Koichi; Watanabe, Yasuhiro

doi:10.1111/j.1476-5381.1992.tb13407.x

Cited by 35 publications

(17 citation statements)

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“…A similar effect (IC 50 ϭ 2.3 M) has been previously noted using amiodarone on I K(ATP) induced by ATP depletion or by bimakalim in inside-out membrane patches of rat ventricular cells (Holmes et al, 2000). However, other studies showed a lower potency (IC 50 ϭ 19 M) of amiodarone on the K ϩ conductance induced by ATP depletion in rat cardiocytes or a lack of effect on I K(ATP) induced by the K ϩ channel opener KRN2391 in Xenopus oocytes (Sakuta et al, 1992). The reason for this discrepancy remains unclear, but the difference in results might have been due to the cell type or the experimental conditions.…”

Section: Discussionmentioning

confidence: 82%

Inhibition of G Protein-Coupled and ATP-Sensitive Potassium Currents by 2-Methyl-3-(3,5-diiodo-4-carboxymethoxybenzyl)benzofuran (KB130015), an Amiodarone Derivative

Brandts

Borchard²,

Mačianskienė³

et al. 2003

J Pharmacol Exp Ther

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Section: Discussionmentioning

confidence: 82%

Inhibition of G Protein-Coupled and ATP-Sensitive Potassium Currents by 2-Methyl-3-(3,5-diiodo-4-carboxymethoxybenzyl)benzofuran (KB130015), an Amiodarone Derivative

Brandts

Borchard²,

Mačianskienė³

et al. 2003

J Pharmacol Exp Ther

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“…Macmillan Press Ltd, 1993 enclosed oocytes (not treated with collagenase) were used for all experiments in the present study. applied to each oocyte by superfusion as described previously (Sakuta et al, 1992a).…”

Section: Methodsmentioning

confidence: 99%

“…TMB-8 is known to block not only the ATP-sensitive K+ channel in insulin-secreting cells (Szewczyk et al, 1992) but also the voltage-dependent Na+ channel and the voltagedependent Ca2+ channel (Himmel & Raven, 1990 (Sakuta et al, 1992a). The effect of the above antiarrhythmic drugs on the KRN2391-induced current was examined.…”

Section: Drugs and Agents Usedmentioning

confidence: 99%

“…The oocyte of Xenopus laevis has an endogenous K+ channel which is activated by K+ channel openers such as cromakalim and pinacidil (Honore & Lazdunski, 1991) and KRN2391 (Sakuta et al, 1992a). Since this oocyte K+ channel is inactivated by glibenclamide (Honore & Lazdunski, 1991) but not by charybdotoxin (an inhibitor of Ca2+ -activated K+ channel) or dendrotoxin (an inhibitor of voltage-dependent K+ channel) (Honore & Lazdunski, 1991), the K+ channel appears to belong to the family of ATPsensitive K+ channels, though its sensitivity to ATP is not yet proven by single channel studies.…”

Section: Introductionmentioning

confidence: 99%

“…nylamine potently block glibenclamide-sensitive K+ channels in Xenopus oocytes with IC50 values of less than 50 JIM (Sakuta et al, 1992a). The suppression of ATP/glibenclamide-sensitive K + channels may be involved in either favourable or unfavourable clinical effects of some antiarrhythmic drugs (see Discussion).…”

Section: Introductionmentioning

confidence: 99%

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Antiarrhythmic drugs, clofilium and cibenzoline are potent inhibitors of glibenclamide‐sensitive K⁺ currents in Xenopus oocytes

Sakuta¹,

Okamoto²,

Watanabe³

1993

British J Pharmacology

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Influence of alpha- and beta-adrenoceptor antagonists on ventricular fibrillation in ischemic rat hearts

Tölg

Kurz

Ungerer³

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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Although it is generally accepted that adrenergic influences contribute to arrhythmias during myocardial ischemia, it is still a matter of debate whether these arrhythmogenic effects are mediated via alpha- or beta-adrenergic receptors and which particular receptor subtype is involved. Controversial results may be due to ancillary properties of the adrenergic receptor antagonists used to resolve this question. Therefore, we compared the influence of various, structurally different alpha- and beta-adrenoceptor blocking agents on the occurrence of ventricular fibrillation in rat isolated hearts. Regional ischemia was induced by ligature of the left coronary artery and ECG was monitored over 30 min of coronary occlusion. Myocardial ischemia precipitated ventricular fibrillation in a well reproducible manner with an incidence of about 80% in control hearts. Racemic propranolol (0.1-1 micromol/l) concentration-relatedly reduced the incidence of ventricular fibrillation from 71% in controls to 10%, whereas the beta-adrenoceptor blocking agents atenolol (10 micromol/l) and timolol (1 micromol/l) did not influence the occurrence of arrhythmias. Moreover, both stereoisomers of propranolol were equipotent in suppressing ischemia-induced ventricular fibrillation, indicating an action of propranolol independent of its beta-adrenoceptor blocking properties. Unselective antagonism of alpha-adrenoceptors by phentolamine decreased the incidence of ventricular fibrillation from 90% to 58% at 0.1 micromol/l and totally suppressed ventricular fibrillation at 1 micromol/l. The alpha1-selective antagonists prazosin and HEAT concentration-dependently (0.1-10 micromol/l) reduced the incidence of ventricular fibrillation from 83% to 0%, whereas the alpha2-selective antagonist RX 821002 revealed no antiarrhythmic effect. Furthermore, subtype specific antagonism of alpha1A-adrenoceptors by WB 4101 clearly reduced the occurrence of ventricular fibrillation in a concentration-dependent manner (0.01-1 micromol/l) from 66% to 17%. Conversely, CEC, known to block the alpha1B-adrenoceptor subtype, possessed no antifibrillatory effect. In conclusion, the contribution of catecholamines to ischemia-induced arrhythmias in rat isolated heart is primarily mediated via WB 4101-sensitive alpha1-adrenergic activation. Beta- and alpha2-adrenoceptor blockade did not affect ventricular fibrillation in this model. The antifibrillatory action of propranolol was rather due to ancillary properties of this agent.

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Blockade by antiarrhythmic drugs of glibenclamide‐sensitive K⁺ channels in Xenopus oocytes

Cited by 35 publications

References 30 publications

Inhibition of G Protein-Coupled and ATP-Sensitive Potassium Currents by 2-Methyl-3-(3,5-diiodo-4-carboxymethoxybenzyl)benzofuran (KB130015), an Amiodarone Derivative

Inhibition of G Protein-Coupled and ATP-Sensitive Potassium Currents by 2-Methyl-3-(3,5-diiodo-4-carboxymethoxybenzyl)benzofuran (KB130015), an Amiodarone Derivative

Antiarrhythmic drugs, clofilium and cibenzoline are potent inhibitors of glibenclamide‐sensitive K⁺ currents in Xenopus oocytes

Influence of alpha- and beta-adrenoceptor antagonists on ventricular fibrillation in ischemic rat hearts

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Blockade by antiarrhythmic drugs of glibenclamide‐sensitive K+ channels in Xenopus oocytes

Cited by 35 publications

References 30 publications

Inhibition of G Protein-Coupled and ATP-Sensitive Potassium Currents by 2-Methyl-3-(3,5-diiodo-4-carboxymethoxybenzyl)benzofuran (KB130015), an Amiodarone Derivative

Inhibition of G Protein-Coupled and ATP-Sensitive Potassium Currents by 2-Methyl-3-(3,5-diiodo-4-carboxymethoxybenzyl)benzofuran (KB130015), an Amiodarone Derivative

Antiarrhythmic drugs, clofilium and cibenzoline are potent inhibitors of glibenclamide‐sensitive K+ currents in Xenopus oocytes

Influence of alpha- and beta-adrenoceptor antagonists on ventricular fibrillation in ischemic rat hearts

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Blockade by antiarrhythmic drugs of glibenclamide‐sensitive K⁺ channels in Xenopus oocytes

Antiarrhythmic drugs, clofilium and cibenzoline are potent inhibitors of glibenclamide‐sensitive K⁺ currents in Xenopus oocytes