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001-es BibID:	BIBFORM030257
035-os BibID:	WOS:000169039300004
Első szerző:	Magyar János (élettanász)
Cím:	Effects of the antiarrhythmic agent EGIS-7229 (S 21407) on calcium and potassium currents in canine ventricular cardiomyocytes / János Magyar, Tamás Bányász, László Fülöp, Norbert Szentandrássy, Ágnes Körtvély, Anikó Kovács, Gábor Szénási, Péter P. Nánási
Dátum:	2001
ISSN:	0028-1298
Megjegyzések:	Based on earlier pharmacological studies performed using conventional microelectrodes EGIS-7229 (S 21407), the novel antiarrhythmic candidate, was suggested to have a combined mode of action in cardiac tissues isolated from various mammalian species. In order to characterize the electrophysiological effects of the compound, its effects on calcium and potassium currents of isolated canine ventricular cardiomyocytes were studied in the present work using the whole cell configuration of the patch clamp technique. L-type Ca current (I-Ca) was significantly depressed by EGIS-7229 at concentrations of 3 muM or higher with no concomitant changes in the voltage-dependence of activation and time course of inactivation of I-Ca. The drug reversibly suppressed the rapid component of the delayed rectifier K current (I-Kr) in a concentration-dependent manner, having a K-0.5 value of 1.1+/-0.1 muM and a slope factor of close to unity (1.23+/-0.16), indicating that probably one single binding site of high affinity may be involved in binding of EGIS-7229 to the I-Kr channel. In contrast, no changes in the slow component of the delayed rectifier K current (I-Ks,) was observed with the compound up to the concentration of 100 muM, even if the current was fully activated by 8-bromo-cAMP. At a concentration of 10 muM or higher, EGIS-7229 caused also a moderate but significant reduction in the inward rectifier K current (I-K1) and the transient outward K current (I-to) with no change in the voltage-dependence of activation and steady-state inactivation of I-to. Present results indicate that EGIS-7229 can be considered as a selective I-Kr blocker at low (1 muM) concentration; however, its combined (class III + IV) mechanism of action is evident at concentrations of 3 muM or higher. Suppression of I-Ca may explain the lack of development of early afterdepolarizations in the presence of EGIS-7229, predicting a relatively safe clinical application in contrast to pure class III compounds.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Naunyn-Schmiedebergs Archives of Pharmacology. - 363 : 6 (2001), p. 604-611. -
További szerzők:	Bányász Tamás (1960-) (élettanász) Fülöp László (1976-) (kardiológus) Szentandrássy Norbert (1976-) (élettanász) Körtvély Ágnes Kovács Anikó Szénási Gábor Nánási Péter Pál (1956-) (élettanász)
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM030256
035-os BibID:	WOS:000178499200009
Első szerző:	Magyar János (élettanász)
Cím:	Electrophysiological effects of risperidone in mammalian cardiac cells / János Magyar, Tamás Bányász, Zsolt Bagi, Pál Pacher, Norbert Szentandrássy, László Fülöp, Valéria Kecskeméti, Péter P. Nánási
Dátum:	2002
ISSN:	0028-1298
Megjegyzések:	In this study, the effects of risperidone, the widely used antipsychotic drug, on isolated canine ventricular myocytes and guinea-pig papillary muscles were analyzed using conventional microelectrode and whole cell voltage-clamp techniques. Risperidone concentration-dependently lengthened action potential duration in guinea-pig papillary muscles (EC50=0.29 +/- 0.02 muM) and single canine ventricular myocytes (EC50=0.48 +/- 0.14 muM). This effect was reversible, showed reverse rate dependence, and it was most prominent on the terminal portion of repolarization. No significant effect of risperidone on the resting membrane potential, action potential amplitude or maximum rate of depolarization was observed. In voltage-clamped canine ventricular myocytes risperidone caused concentration-dependent block of the rapid component of the delayed rectifier K+ current (1(Kr)), measured as outward current tails at -40 mV with an IC50 of 0.92 +/- 0.26 muM. Suppression of I-Kr was not associated with changes in activation or deactivation kinetics. High concentration of risperidone (10 muM) suppressed also the slow component of the delayed rectifier K+ current (I-Ks) by 9.6 +/- 1.5% at +50 mV. These effects of risperidone developed rapidly and were readily reversible. Risperidone had no significant effect on the amplitude of other K+ currents (I-K1 and I-to). The inhibition of cardiac I-Kr current by risperidone may explain the cardiac side-effects observed occasionally with the drug. Our results suggest that risperidone displays class III antiarrhythmic properties, and as such, may produce QTc prolongation, especially in patients with long QT syndrome. Therefore, in psychotic patients having also cardiac disorders, ECG control may be suggested during risperidone therapy.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Naunyn-Schmiedebergs Archives of Pharmacology. - 366 : 4 (2002), p. 350-356. -
További szerzők:	Bányász Tamás (1960-) (élettanász) Bagi Zsolt (1974-) (orvos) Pacher Pál Szentandrássy Norbert (1976-) (élettanász) Fülöp László (1976-) (kardiológus) Kecskeméti Valéria Nánási Péter Pál (1956-) (élettanász)
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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