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1.

001-es BibID:BIBFORM001042
Első szerző:Acsai Károly
Cím:Effect of partial blockade of the Na+/Ca2+ - exchanger on Ca2+ handling in isolated rat ventricular myocytes / Károly Acsai, Attila Kun, Attila S. Farkas, Ferenc Fülöp, Norbert Nagy, Marianna Balázs, Norbert Szentandrássy, Péter P. Nánási, Julius Gy. Papp, András Varró, András Tóth
Dátum:2007
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal of Pharmacology. - 576 : 1-3 (2007), p. 1-6. -
További szerzők:Kun Attila Farkas S. Attila Fülöp Ferenc Nagy Norbert (1977-) (kísérletes farmakológus) Balázs Marianna Szentandrássy Norbert (1976-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Tóth András (farmakológus)
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2.

001-es BibID:BIBFORM004074
Első szerző:Birinyi Péter (élettanász)
Cím:The Na+/Ca2+ exchange blocker SEA0400 fails to enhance cytosolic Ca2+ transient and contractility in canine ventricular cardiomyocytes / Birinyi P., Tóth A., Jóna I., Acsai K., Almássy J., Nagy N., Prorok J., Gherasim I., Papp Z., Hertelendi Z., Szentandrássy N., Bányász T., Fülöp F., Papp J. G., Varró A., Nánási P. P., Magyar J.
Dátum:2008
Megjegyzések:Aims This study was designed to evaluate the effects of the Na+/Ca2+ exchange (NCX) inhibitor SEA0400 on Ca2+ handling in isolated canine ventricular myocytes. Methods and results Intracellular Ca2+ ([Ca2+](i)) transients, induced by either field stimulation or caffeine flush, were monitored using Ca2+ indicator dyes. [Ca2+](i)-dependent modulation of the inhibitory effect of SEA0400 on NCX was characterized by the changes in Ni2+-sensitive current in voltage-clamped myocytes. Sarcoplasmic reticulum (SR) Ca2+ release and uptake were studied in SIR membrane vesicles. Gating properties of single-ryanodine receptors were analysed in lipid bilayers. Ca2+ sensitivity of the contractile machinery was evaluated in chemically skinned myocytes. In myocytes paced at 1 Hz, neither diastolic [Ca2+](i) nor the amplitude of [Ca2+](i) transients was significantly altered by SEA0400 up to the concentration of 1 mu M, which was shown to inhibit the exchange current. The blocking effect of SEA0400 on NCX decreased with increasing [Ca2+](i), and it was more pronounced in reverse than in forward mode operation at every [Ca2+](i) examined. The rate of decay of the caffeine-induced [Ca2+](i) transients was decreased significantly by 1 mu M SEA0400; however, this effect was only a fraction of that observed with 10 mM NiCl2. Neither SR Ca2+ release and uptake nor cell shortening and Ca2+ sensitivity of the contractile proteins were influenced by SEA0400. Conclusion The lack of any major SEA0400-induced shift in Ca2+ transients or contractility of myocytes can well be explained by its limited inhibitory effect on NCX (further attenuated by elevated [Ca2+](i) levels) and a concomitant reduction in Ca2+ influx due to the predominantly reverse mode blockade of NCX and suppression of L-type Ca2+ current.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cardiovascular Research. - 78 : 3 (2008), p. 476-484. -
További szerzők:Tóth András (farmakológus) Jóna István (1948-) (élettanász, fizikus) Acsai Károly Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Nagy Norbert (1977-) (kísérletes farmakológus) Prorok János Gherasim, Iuliana Papp Zoltán (1965-) (kardiológus, élettanász) Hertelendi Zita (1978-) (orvos) Szentandrássy Norbert (1976-) (élettanász) Bányász Tamás (1960-) (élettanász) Fülöp Ferenc Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász) Magyar János (1961-) (élettanász)
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3.

001-es BibID:BIBFORM086081
035-os BibID:(WoS)000513023203220
Első szerző:Horváth Balázs (élettanász)
Cím:Late Sodium Current in Canine, Guinea Pig and Human Left Ventricular Myocardium / Balazs Horvath, Tamas Hezso, Norbert Szentandrássy, Kornel Kistamas, Tamas Arpadffy-Lovas, Roland Veress, Csaba B. Dienes, Dora Baranyai, Laszlo Virag, Norbert Nagy, Istvan Baczko, Janos Magyar, Tamas Banyasz, Andras Varro, Peter P. Nanasi
Dátum:2020
ISSN:0006-3495
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Biophysical Journal. - 118 : Suppl. 1 (2020), p. 494a-495a. -
További szerzők:Hézső Tamás (1993-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Kistamás Kornél (1986-) (biológus) Árpádffy-Lovas Tamás Veress Roland (1992-) (molekuláris biológus) Dienes Csaba (1995-) (gyógyszerész) Baranyai Dóra Virág László (élettanász Szeged) Nagy Norbert (1977-) (kísérletes farmakológus) Baczkó István Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
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4.

001-es BibID:BIBFORM083023
035-os BibID:(WoS)000522138400002 (Scopus)85078193947 (PubMed)31958464
Első szerző:Horváth Balázs (élettanász)
Cím:Late sodium current in human, canine and guinea pig ventricular myocardium / Balázs Horváth, Tamás Hézső, Norbert Szentandrássy, Kornél Kistamás, Tamás Árpádffy-Lovas, Richárd Varga, Péter Gazdag, Roland Veress, Csaba Dienes, Dóra Baranyai, János Almássy, László Virág, Norbert Nagy, István Baczkó, János Magyar, Tamás Bányász, András Varró, Péter P. Nánási
Dátum:2020
ISSN:0022-2828
Megjegyzések:Although late sodium current (INa-late) has long been known to contribute to plateau formation of mammalian cardiac action potentials, lately it was considered as possible target for antiarrhythmic drugs. However, many aspects of this current are still poorly understood. The present work was designed to study the true profile of INa-late in canine and guinea pig ventricular cells and compare them to INa-late recorded in undiseased human hearts. INa-late was defined as a tetrodotoxin-sensitive current, recorded under action potential voltage clamp conditions using either canonic- or self-action potentials as command signals. Under action potential voltage clamp conditions the amplitude of canine and human INa-late monotonically decreased during the plateau (decrescendo-profile), in contrast to guinea pig, where its amplitude increased during the plateau (crescendo profile). The decrescendo-profile of canine INa-late could not be converted to a crescendo-morphology by application of ramp-like command voltages or command action potentials recorded from guinea pig cells. Conventional voltage clamp experiments revealed that the crescendo INa-late profile in guinea pig was due to the slower decay of INa-late in this species. When action potentials were recorded from multicellular ventricular preparations with sharp microelectrode, action potentials were shortened by tetrodotoxin, which effect was the largest in human, while smaller in canine, and the smallest in guinea pig preparations. It is concluded that important interspecies differences exist in the behavior of INa-late. At present canine myocytes seem to represent the best model of human ventricular cells regarding the properties of INa-late. These results should be taken into account when pharmacological studies with INa-late are interpreted and extrapolated to human. Accordingly, canine ventricular tissues or myocytes are suggested for pharmacological studies with INa-late inhibitors or modifiers. Incorporation of present data to human action potential models may yield a better understanding of the role of INa-late in action potential morphology, arrhythmogenesis, and intracellular calcium dynamics.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Late Na+ current
Ventricular repolarization
Action potential voltage clamp
Dog myocytes
Human myocytes
Megjelenés:Journal of Molecular and Cellular Cardiology. - 139 (2020), p. 14-23. -
További szerzők:Hézső Tamás (1993-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Kistamás Kornél (1986-) (biológus) Árpádffy-Lovas Tamás Varga Richárd Gazdag Péter Veress Roland (1992-) (molekuláris biológus) Dienes Csaba (1995-) (gyógyszerész) Baranyai Dóra Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Virág László (élettanász Szeged) Nagy Norbert (1977-) (kísérletes farmakológus) Baczkó István Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:GINOP-2.3.2.-15-2016-00040
GINOP
EFOP-3.6.2-16-2017-00006
EFOP
ÚNKP-19-4
Egyéb
ÚNKP-19-2
Egyéb
NKFIH-K115397
NKFIH
NKFIH-PD120794
NKFIH
NKFIH-FK128116
NKFIH
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5.

001-es BibID:BIBFORM051689
035-os BibID:WOS:000326178500011
Első szerző:Jost Norbert
Cím:Ionic mechanisms limiting cardiac repolarization reserve in humans compared to dogs / Norbert Jost, László Virág, Philippe Comtois, Balázs Ördög, Viktória Szuts, György Seprényi, Miklós Bitay, Zsófia Kohajda, István Koncz, Norbert Nagy, Tamás Szél, János Magyar, Mária Kovács, László G. Puskás, Csaba Lengyel, Erich Wettwer, Ursula Ravens, Péter P. Nánási, Julius Gy. Papp, András Varró, Stanley Nattel
Dátum:2013
ISSN:0022-3751
Megjegyzések:Abstract The species-specific determinants of repolarization are poorly understood. Thisstudy compared the contribution of various currents to cardiac repolarization in canine andhuman ventricle.Conventional microelectrode,whole-cell patch-clamp,molecular biological andmathematical modelling techniques were used. Selective IKr block (50?100 nmol l?1 dofetilide)lengthened AP duration at 90% of repolarization (APD90) >3-fold more in human than dog,suggesting smaller repolarization reserve in humans. Selective IK1 block (10 ?mol l?1 BaCl2) andIKs block (1 ?mol l?1 HMR-1556) increased APD90 more in canine than human right ventricularpapillary muscle. Ion current measurements in isolated cardiomyocytes showed that IK1 and IKsdensities were 3- and 4.5-fold larger in dogs than humans, respectively. IKr density and kineticswere similar in human versus dog. ICa and Ito were respectively ?30% larger and ?29% smallerin human, and Na+?Ca2+ exchange current was comparable. Cardiac mRNA levels for the main IK1 ion channel subunit Kir2.1 and the IKs accessory subunit minK were significantly lower, butmRNA expression of ERG and KvLQT1 (IKr and IKs ?-subunits) were not significantly different,in human versus dog. Immunostaining suggested lower Kir2.1 and minK, and higher KvLQT1protein expression in human versus canine cardiomyocytes. IK1 and IKs inhibition increased theAPD-prolonging effect of IKr block more in dog (by 56% and 49%, respectively) than human(34 and 16%), indicating that both currents contribute to increased repolarization reserve inthe dog. A mathematical model incorporating observed human?canine ion current differencesconfirmed the role of IK1 and IKs in repolarization reserve differences. Thus, humans show greaterrepolarization-delaying effects of IKr block than dogs, because of lower repolarization reservecontributions from IK1 and IKs, emphasizing species-specific determinants of repolarization andthe limitations of animal models for human disease.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
L-type calcium current
action potential
dog heart
human heart
repolarization
Megjelenés:Journal of Physiology-London. - 591 : 17 (2013), p. 4189-4206. -
További szerzők:Virág László (élettanász Szeged) Comtois, Philippe Ördög Balázs Szuts Viktória Seprényi György Bitay Miklós Kohajda Zsófia Koncz István (Szeged) Nagy Norbert (1977-) (kísérletes farmakológus) Szél Tamás Magyar János (1961-) (élettanász) Kovács Mária (Szeged) Puskás László G. Lengyel Csaba (Szeged) Wettwer, Erich Ravens, Ursula Nánási Péter Pál (1956-) (élettanász) Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Nattel, Stanley
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6.

001-es BibID:BIBFORM067775
Első szerző:Kohajda Zsófia
Cím:The Effect of a Novel Highly Selective Inhibitor of the Sodium/Calcium Exchanger (NCX) on Cardiac Arrhythmias in In Vitro and In Vivo Experiments / Zsófia Kohajda, Nikolett Farkas-Morvay, Norbert Jost, Norbert Nagy, Amir Geramipour, András Horváth, Richárd S. Varga, Tibor Hornyik, Claudia Corici, Károly Acsai, Balázs Horváth, János Prorok, Balázs Ördög, Szilvia Déri, Dániel Tóth, Jouko Levijoki, Piero Pollesello, Tuula Koskelainen, Leena Otsomaa, András Tóth, István Baczkó, István Leprán, Péter P. Nánási, Gy. Julius Papp, András Varró, László Virág
Dátum:2016
ISSN:1932-6203
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Plos One. - 11 : 11 (2016), p. 1-28. -
További szerzők:Farkas-Morvay Nikolett Jost Norbert Nagy Norbert (1977-) (kísérletes farmakológus) Geramipour, Amir Horváth András (1976-) (vegyész) Varga Richárd Sándor Hornyik Tibor Corici, Claudia Acsai Károly Horváth Balázs (1981-) (élettanász) Prorok János Ördög Balázs Déri Szilvia Tóth Dániel Levijoki, Jouko Pollesello, Piero Koskelainen, Tuula Otsomaa, Leena Tóth András (farmakológus) Baczkó István Leprán István Nánási Péter Pál (1956-) (élettanász) Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Virág László (élettanász Szeged)
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7.

001-es BibID:BIBFORM105581
035-os BibID:(cikkazonosító)14651 (WOS)000897324400001 (Scopus)85143732443 (PubMed)36498977
Első szerző:Nagy Norbert (kísérletes farmakológus)
Cím:Antiarrhythmic and Inotropic Effects of Selective Na+/Ca2+ Exchanger Inhibition : What Can We Learn from the Pharmacological Studies? / Nagy Norbert, Tóth Noémi, Nánási Péter P.
Dátum:2022
ISSN:1422-0067
Megjegyzések:Life-long stable heart function requires a critical balance of intracellular Ca2+. Several ion channels and pumps cooperate in a complex machinery that controls the influx, release, and efflux of Ca2+. Probably one of the most interesting and most complex players of this crosstalk is the Na+/Ca2+ exchanger, which represents the main Ca2+ efflux mechanism; however, under some circumstances, it can also bring Ca2+ into the cell. Therefore, the inhibition of the Na+/Ca2+ exchanger has emerged as one of the most promising possible pharmacological targets to increase Ca2+ levels, to decrease arrhythmogenic depolarizations, and to reduce excessive Ca2+ influx. In line with this, as a response to increasing demand, several more or less selective Na+/Ca2+ exchanger inhibitor compounds have been developed. In the past 20 years, several results have been published regarding the effect of Na+/Ca2+ exchanger inhibition under various circumstances, e.g., species, inhibitor compounds, and experimental conditions; however, the results are often controversial. Does selective Na+/Ca2+ exchanger inhibition have any future in clinical pharmacological practice? In this review, the experimental results of Na+/Ca2+ exchanger inhibition are summarized focusing on the data obtained by novel highly selective inhibitors.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
heart
Na+/Ca2+ exchanger
arrhythmia
Ca2+-handling
inotropy
Megjelenés:International Journal Of Molecular Sciences. - 23 : 23 (2022), p. 14651. -
További szerzők:Tóth Noémi Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:FK-129117
OTKA
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8.

001-es BibID:BIBFORM081896
Első szerző:Nagy Norbert (kísérletes farmakológus)
Cím:Selective Na+/Ca2+ exchanger inhibition prevents Ca2+ overload-induced triggered arrhythmias / Norbert Nagy, Anita Kormos, Zsófia Kohajda, Áron Szebeni, Judit Szepesi, Piero Pollesello, Jouko Levijoki, Károly Acsai, László Virág, Péter P. Nánási, Julius Gy. Papp, András Varró, András Tóth
Dátum:2014
ISSN:0007-1188
Megjegyzések:Background and Purpose Augmented Na+/Ca2+ exchanger (NCX) activity may play a crucial role in cardiac arrhythmogenesis; however, data regarding the anti?arrhythmic efficacy of NCX inhibition are debatable. Feasible explanations could be the unsatisfactory selectivity of NCX inhibitors and/or the dependence of the experimental model on the degree of Ca2+i overload. Hence, we used NCX inhibitors SEA0400 and the more selective ORM10103 to evaluate the efficacy of NCX inhibition against arrhythmogenic Ca2+i rise in conditions when [Ca2+]i was augmented via activation of the late sodium current (INaL) or inhibition of the Na+/K+ pump. Experimental Approach Action potentials (APs) were recorded from canine papillary muscles and Purkinje fibres by microelectrodes. NCX current (INCX) was determined in ventricular cardiomyocytes utilizing the whole?cell patch clamp technique. Ca2+i transients (CaTs) were monitored with a Ca2+?sensitive fluorescent dye, Fluo?4. Key Results Enhanced INaL increased the Ca2+ load and AP duration (APD). SEA0400 and ORM10103 suppressed INCX and prevented/reversed the anemone toxin II (ATX?II)?induced [Ca2+]i rise without influencing APD, CaT or cell shortening, or affecting the ATX?II?induced increased APD. ORM10103 significantly decreased the number of strophanthidin?induced spontaneous diastolic Ca2+ release events; however, SEA0400 failed to restrict the veratridine?induced augmentation in Purkinje?ventricle APD dispersion. Conclusions and Implications Selective NCX inhibition ? presumably by blocking revINCX (reverse mode NCX current) ? is effective against arrhythmogenesis caused by [Na+]i?induced [Ca2+]i elevation, without influencing the AP waveform. Therefore, selective INCX inhibition, by significantly reducing the arrhythmogenic trigger activity caused by the perturbed Ca2+i handling, should be considered as a promising anti?arrhythmic therapeutic strategy.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:British Journal of Pharmacology. - 171 : 24 (2014), p. 5665-5681. -
További szerzők:Kormos Anita Kohajda Zsófia Szebeni Áron Szepesi Judit Pollesello, Piero Levijoki, Jouko Acsai Károly Virág László (élettanász Szeged) Nánási Péter Pál (1956-) (élettanász) Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Tóth András (farmakológus)
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9.

001-es BibID:BIBFORM053175
035-os BibID:WOS:000326116400010
Első szerző:Nagy Norbert (kísérletes farmakológus)
Cím:[Ca2+]i-induced augmentation of the inward rectifier potassium current (IK1) in canine and human ventricular myocardium / Norbert Nagy, Károly Acsai, Anita Kormos, Zsuzsanna Sebők, Attila S. Farkas, Norbert Jost, Péter P. Nánási, Julius Gy. Papp, András Varró, András Tóth
Dátum:2013
ISSN:0031-6768
Megjegyzések:The inward rectifier K? current (IK1) plays an important role in terminal repolarization and stabilization of the resting potential in cardiac cells. Although IK1 was shown to be sensitive to changes in intracellular Ca?? concentration ([Ca??]i), the nature of this Ca?? sensitivity-in spite of its deep influence on action potential morphology-is controversial. Therefore, we aimed to investigate the effects of a nonadrenergic rise in [Ca??]i on the amplitude of IK1 in canine and human ventricular myocardium and its consequences on cardiac repolarization. IK1, defined as the current inhibited by 10 ?M Ba??, was significantly increased in isolated canine myocytes following a steady rise in [Ca??]i. Enhanced IK1 was also observed when [Ca??]i was not buffered by ethylene glycol tetraacetic acid, and [Ca??]I transients were generated. This [Ca??]i-dependent augmentation of IK1 was largely attenuated after inhibition of CaMKII by 1 ?M KN-93. Elevation of [Ca??]o in multicellular canine and human ventricular preparations resulted in shortening of action potentials and acceleration of terminal repolarization. High [Ca??]o enhanced the action potential lengthening effect of the Ba(2+)-induced IK1 blockade and attenuated the prolongation of action potentials following a 0.3-?M dofetilide-induced IKr blockade. Blockade of IKs by 0.5 ?M HMR-1556 had no significant effect on APD90 in either 2 mM or 4 mM [Ca??]o. It is concluded that high [Ca??]i leads to augmentation of the Ba??-sensitive current in dogs and humans, regardless of the mechanism of the increase. This effect seems to be at least partially mediated by a CaMKII-dependent pathway and may provide an effective endogenous defense against cardiac arrhythmias induced by Ca?? overload.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Canine/human myocardium
Inward rectifier K+ current (IK1)
Cytosolic Ca2+
Action potential duration
Ventricular repolarization
Ba2+
Megjelenés:Pflugers Archiv-European Journal of Physiology. - 465 : 11 (2013), p. 1621-1635. -
További szerzők:Acsai Károly Kormos Anita Sebők Zsuzsanna Farkas Attila (1961-) (farmakológus) Jost Norbert Nánási Péter Pál (1956-) (élettanász) Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Tóth András (farmakológus)
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10.

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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