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001-es BibID:	BIBFORM016600
Első szerző:	Bárándi László (élettanász)
Cím:	Reverse rate-dependent changes are determined by baseline action potential duration in mammalian and human ventricular preparations / Bárándi László, Virág László, Jost Norbert, Horváth Zoltán, Koncz István, Papp Rita, Harmati Gábor, Horváth Balázs, Szentandrássy Norbert, Bányász Tamás, Magyar János, Zaza Antonio, Varró András, Nánási Péter P.
Dátum:	2010
ISSN:	0300-8428
Megjegyzések:	Class III antiarrhythmic agents exhibit reverse rate-dependent lengthening of the action potential duration (APD). In spite of the several theories developed so far to explain this reverse rate-dependency (RRD), its mechanism has not yet been clarified. The aim of the present work was to further elucidate the mechanisms responsible for RRD in mammalian ventricular myocardium. Action potentials were recorded using conventional sharp microelectrodes from human, canine, rabbit and guinea pig ventricular myocardium in a rate-dependent manner varying the cycle length (CL) between 0.3 and 5 s. Rate-dependent drug effects were studied using agents known to lengthen or shorten action potentials, and these drug-induced changes in APD were correlated with baseline APD values. Both drug-induced lengthening (by dofetilide, sotalol, E-4031, BaCl2, veratrine, BAY K 8644) and shortening (by mexiletine, tetrodotoxin, lemakalim) of action potentials displayed RRD, i.e., changes in APD were greater at longer than at shorter CLs. In rabbit, where APD is a biphasic function of CL, the drug-induced APD changes were proportional to baseline APD values but not to CL. Similar results were obtained when repolarization was modified by injection of inward or outward current pulses in isolated canine cardiomyocytes. In each case the change in APD was proportional to baseline APD (i.e., that measured before the superfusion of drug or injection of current). Also, the net membrane current (Inet), determined from the action potential waveform at the middle of the plateau, was inversely proportional to APD and consequently with to CL. The results indicate that RRD is a common characteristic of all the drugs tested regardless of the modified ion current species. Thus, drug-induced RRD can be considered as an intrinsic property of cardiac membranes based on the inverse relationship between Inet and APD.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Ventricular repolarization Action potential duration Reverse rate dependence Membrane current Human myocardium Mammalian cardiac cells egyetemen (Magyarországon) készült közlemény
Megjelenés:	Basic Research In Cardiology. - 105 : 3 (2010), p. 315-323. -
További szerzők:	Virág László (élettanász Szeged) Jost Norbert Horváth Zoltán Koncz István (Szeged) Papp Rita Harmati Gábor (1983-) (élettanász) Horváth Balázs (1981-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Bányász Tamás (1960-) (élettanász) Magyar János (1961-) (élettanász) Zaza, Antonio Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
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001-es BibID:	BIBFORM009105
Első szerző:	Nagy Norbert (kísérletes farmakológus)
Cím:	Does small-conductance calcium-activated potassium channel contribute to cardiac repolarization? / Nagy, N., Szuts, V., Horvath, Z., Seprenyi, G., Farkas, A. S., Acsai, K., Prorok, J., Bitay, M., Kun, A., Pataricza, J., Papp, J. G., Nanasi, P. P., Varro, A., Toth, A.
Dátum:	2009
ISSN:	0022-2828 (Print)
Megjegyzések:	Small-conductance calcium-activated potassium channels (SK channels) have a significant role in neurons. Since they directly integrate calcium handling with repolarization, in heart their role would be particularly important. However, their contribution to cardiac repolarization is still unclear. A previous study reported a significant lengthening effect of apamin, a selective SK channel inhibitor, on the action potential duration in atrial and ventricular mouse cardiomyocytes and human atrial cells. They concluded that these channels provide an important functional link between intracellular calcium handling and action potential kinetics. These findings seriously contradict our studies on cardiac "repolarization reserve", where we demonstrated that inhibition of a potassium current is not likely to cause excessive APD lengthening, since its decrease is mostly compensated by a secondary increase in other, unblocked potassium currents. To clarify this contradiction, we reinvestigated the role of the SK current in cardiac repolarization, using conventional microelectrode and voltage-clamp techniques in rat and dog atrial and ventricular multicellular preparations, and in isolated cardiomyocytes. SK2 channel expression was confirmed with immunoblot technique and confocal microscopy. We found, that while SK2 channels are expressed in the myocardium, a full blockade of these channels by 100 nM apamin--in contrast to the previous report--did not cause measurable electrophysiological changes in mammalian myocardium, even when the repolarization reserve was blunted. These results clearly demonstrate that in rat, dog and human ventricular cells under normal physiological conditions--though present--SK2 channels are not active and do not contribute to action potential repolarization.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Journal of Molecular and Cellular Cardiology. - 47 : 5 (2009), p. 656-663. -
További szerzők:	Szűts Viktória (farmakológus Szeged) Horváth Zoltán Seprényi György Farkas Attila (1961-) (farmakológus) Acsai Károly Prorok János Bitay Miklós Kun Attila Pataricza János Papp Gy. Julius (Szeged) Nánási Péter Pál (1956-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Tóth András (farmakológus)
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