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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:BIBFORM084740
Első szerző:Jost Norbert
Cím:Role of Na+/Ca2+ exchanger (NCX) in cardiac automaticity and ventricular repolarization assessed by ORM-10962, a novel highly selective NCX inhibitor / Jost Norbert László, Kohajda Zsófia, Nagy Norbert, Geramipour Amir Mohammad, Varga Richárd Sándor, Hornyik Tibor, Horváth Balázs, Kormos Anita, Acsai Károly, Levijoki J., Pollesello P., Koskelainen T., Otsomaa L., Tóth András, Baczkó István, Nanasi P. P., Papp Gyula Julius, Virág László, Varró András
Dátum:2016
ISSN:1547-5271
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Heart Rhythm. - 13 : 5 Suppl. (2016), p. S6-S7. -
További szerzők:Kohajda Zsófia Nagy Norbert Geramipour, Amir Varga Richárd Sándor Hornyik Tibor Horváth Balázs (1981-) (élettanász) Kormos Anita Acsai Károly Levijoki, Jouko Pollesello, Piero Koskelainen, Tuula Otsomaa, Leena Tóth András Baczkó István Nánási Péter Pál (1956-) (élettanász) Papp Gy. Julius (Szeged) Virág László (élettanász Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus)
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4.

001-es BibID:BIBFORM051689
035-os BibID:(Scopus)84883281759 (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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5.

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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6.

001-es BibID:BIBFORM009079
Első szerző:Lengyel Csaba (Szeged)
Cím:Role of slow delayed rectifier K+-current in QT prolongation in the alloxan-induced diabetic rabbit heart / Lengyel, C., Virag, L., Kovacs, P. P., Kristof, A., Pacher, P., Kocsis, E., Koltay, Z. M., Nanasi, P. P., Toth, M., Kecskemeti, V., Papp, J. G., Varro, A., Jost, N.
Dátum:2008
ISSN:1748-1716 (Electronic)
Megjegyzések:In diabetes mellitus, several cardiac electrophysiological parameters are known to be affected. In rodent experimental diabetes models, changes in these parameters were reported, but only limited relevant information is available in other species, having cardiac electrophysiological properties more resembling the human, including the rabbit. The present study was designed to analyse the effects of experimental type 1 diabetes on ventricular repolarization and the underlying transmembrane potassium currents in rabbit hearts. METHODS: Diabetes was induced by a single injection of alloxan (145 mg kg(-1) i.v.). After the development of diabetes (3 weeks), electrophysiological studies were performed using whole cell voltage clamp and ECG measurements. RESULTS: The QT(c) interval in diabetic rabbits was moderately but statistically significantly longer than measured in the control animals (155 +/- 1.8 ms vs. 145 +/- 2.8 ms, respectively, n = 9-10, P < 0.05). This QT(c)-lengthening effect of diabetes was accompanied by a significant reduction in the density of the slow delayed rectifier K(+) current, I(Ks) (from 1.48 +/- 0.35 to 0.86 +/- 0.17 pA pF(-1) at +50 mV, n = 19-21, P < 0.05) without changes in current kinetics. No differences were observed either in the density or in the kinetics of the inward rectifier K(+) current (I(K1)), the rapid delayed rectifier K(+) current (I(Kr)), the transient outward current (I(to)) and the L-type calcium current (I(CaL)) between the control and alloxan-treated rabbits. CONCLUSION: It is concluded that type 1 diabetes mellitus, although only moderately, lengthens ventricular repolarization. Diabetes attenuates the repolarization reserve by decreasing the density of I(Ks) current, and thereby may enhance the risk of sudden cardiac death.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Alloxan
Animals
Delayed Rectifier Potassium Channels
Diabetes Mellitus, Experimental
Electrocardiography
Heart
Heart Conduction System
Heart Ventricles
Long QT Syndrome
Male
Patch-Clamp Techniques
Rabbits
Megjelenés:Acta Physiologica (Oxford, England). - 192 : 3 (2008), p. 359-368. -
További szerzők:Virág László (élettanász Szeged) Kovacs Péter Pál (Szeged) Kristóf A. (Szeged) Pacher Pál Kocsis E. Koltay Zs. M. Nánási Péter Pál (1956-) (élettanász) Tóth M. Kecskeméti Valéria Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Jost Norbert
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7.

001-es BibID:BIBFORM001024
Első szerző:Lengyel Csaba (Szeged)
Cím:Diabetes mellitus attenuates the repolarization reserve in mammalian heart / Lengyel Cs., Virág L., Bíró T., Jost N., Magyar J., Biliczki P., Kocsis E., Skoumal R., Nánási P.P., Tóth M., Kecskeméti V., Papp Gy. J., Varró A.
Dátum:2007
ISSN:0008-6363 (Print)
Megjegyzések:In diabetes mellitus several cardiac electrophysiological parameters are known to be affected. In rodent experimental diabetes models changes in these parameters were reported, but no such data are available in other mammalian species including the dog. The present study was designed to analyse the effects of experimental type 1 diabetes on ventricular repolarization and its underlying transmembrane ionic currents and channel proteins in canine hearts. METHODS AND RESULTS: Diabetes was induced by a single injection of alloxan, a subgroup of dogs received insulin substitution. After the development of diabetes (8 weeks) electrophysiological studies were performed using conventional microelectrodes, whole cell voltage clamp, and ECG. Expression of ion channel proteins was evaluated by Western blotting. The QTc interval and the ventricular action potential duration in diabetic dogs were moderately prolonged. This was accompanied by significant reduction in the density of the transient outward K+ current (I(to)) and the slow delayed rectifier K+ current (I(Ks)), to 54.6% and 69.3% of control, respectively. No differences were observed in the density of the inward rectifier K+ current (I(K1)), rapid delayed rectifier K+ current (I(Kr)), and L-type Ca2+ current (I(Ca)). Western blot analysis revealed a reduced expression of Kv4.3 and MinK (to 25+/-21% and 48+/-15% of control, respectively) in diabetic dogs, while other channel proteins were unchanged (HERG, MiRP1, alpha(1c)) or increased (Kv1.4, KChIP2, KvLQT1). Insulin substitution fully prevented the diabetes-induced changes in I(Ks), KvLQT1 and MinK, however, the changes in I(to), Kv4.3, and Kv1.4 were only partially diminished by insulin. CONCLUSION: It is concluded that type 1 diabetes mellitus, although only moderately, lengthens ventricular repolarization, attenuates the repolarization reserve by decreasing I(to) and I(Ks) currents, and thereby may markedly enhance the risk of sudden cardiac death.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cardiovascular Research 73 : 3 (2007), p. 512-520. -
További szerzők:Virág László (élettanász Szeged) Bíró Tamás (1968-) (élettanász) Jost Norbert Magyar János (1961-) (élettanász) Biliczki Péter Kocsis E. Skoumal, R. Nánási Péter Pál (1956-) (élettanász) Tóth M. Kecskeméti Valéria Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus)
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8.

001-es BibID:BIBFORM030270
035-os BibID:(Scopus)17744391778 (WoS)000165611500019
Első szerző:Magyar János (élettanász)
Cím:Effects of endothelin-1 on calcium and potassium currents in undiseased human ventricular myocytes / J. Magyar, N. Iost, Á. Körtvély, T. Bányász, L. Virág, P. Szigligeti, A. Varró, M. Opincariu, J. Szécsi, J. G. Papp, P. P. Nánási
Dátum:2000
ISSN:0031-6768
Megjegyzések:Endothelins have been reported to exert a wide range of electrophysiological effects in mammalian cardiac cells. These results are controversial and human data are not available. Our aim was to study the effects of endothelin-l (ET-1, 8 nmol/l) on the L-type calcium current (ICa-L) and various potassium currents (rapid component of the delayed rectifier, I-Kr; transient outward current, I-to; and the inward rectifier K current, I-K1) in isolated human ventricular cardiomyocytes. Cells were obtained from undiseased donor hearts using collagenase digestion via the segment perfusion technique. The whole-cell configuration of the patch-clamp technique was applied to measure ionic currents at 37 degreesC. ET-1 significantly decreased peak I-Ca,I-L from 10.2+/-0.6 to 6.8+/-0.8 pA/pF at +5 mV (66.7% of control, P <0.05, n=5). This reduction of peak current was accompanied by a lengthening of inactivation. The voltage dependence of steady-state activation and inactivation was not altered by ET-1. I-Kr, measured as tail current amplitudes at -40 mV, decreased from 0.31+/-0.02 to 0.06+/-0.02 pA/pF (20.3% of control, P <0.05, n=4) after exposure to ET-1. ET-I failed to change the peak amplitude of I-to, measured at +50 mV (9.3+/-4.6 and 9.0+/-4.4 pA/pF before and after ET-1, respectively), or steady-state I-K1 amplitude, measured at the end of a 400-ms hyperpolarization to -100 mV (3.6+/-1.4 and 3.7+/-1.4 pA/pF, n=4). The present results indicate that in undiseased human ventricular myocytes ET-1 inhibits both ICa-L and I-Kr; however, the degree of suppression of the two currents is different.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Pflügers Archiv. - 441 : 1 (2000), p. 144-149. -
További szerzők:Iost, N. Körtvély Ágnes Bányász Tamás (1960-) (élettanász) Virág László (élettanász Szeged) Szigligeti Péter Varró András (1954-) (farmakológus, klinikai farmakológus) Opincariu, M. Szécsi János (1955-) (szívsebész) Papp Gy. Julius (Szeged) Nánási Péter Pál (1956-) (élettanász)
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9.

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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10.

001-es BibID:BIBFORM053175
035-os BibID:(Scopus)84887143836 (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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DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

11.

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)
Internet cím:DOI
elektronikus változat
Borító:

12.

001-es BibID:BIBFORM030240
Első szerző:Nagy, Zsolt A.
Cím:Selective inhibition of sodium-calcium exchanger by SEA-0400 decreases early and delayed after depolarization in canine heart / Zsolt A. Nagy, László Virág, András Tóth, Péter Biliczki, Károly Acsai, Tamás Bányász, Péter Nánási, Julius Gy. Papp, András Varro
Dátum:2004
ISSN:0007-1188
Megjegyzések:The sodium-calcium exchanger (NCX) was considered to play an important role in arrhythmogenesis under certain conditions such as heart failure or calcium overload. In the present study, the effect of SEA-0400, a selective inhibitor of the NCX, was investigated on early and delayed afterdepolarizations in canine ventricular papillary muscles and Purkinje fibres by applying conventional microelectrode techniques at 37degreesC. The amplitude of both early and delayed afterdepolarizations was markedly decreased by 1 mum SEA-0400 from 26.6 +/- 2.5 to 14.8 +/- 1.8 mV (n = 9, P < 0.05) and from 12.5 &PLUSMN; 1.7 to 5.9 &PLUSMN; 1.4 mV (n = 3, P < 0.05), respectively. In enzymatically isolated canine ventricular myocytes, SEA-0400 did not change significantly the L-type calcium current and the intracellular calcium transient, studied using the whole-cell configuration of the patch-clamp technique and Fura-2 ratiometric fluorometry. It is concluded that, through the reduction of calcium overload, specific inhibition of the NCX current by SEA-0400 may abolish triggered arrhythmias.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:British Journal of Pharmacology. - 143 : 7 (2004), p. 827-831. -
További szerzők:Virág László (élettanász Szeged) Tóth András (farmakológus) Biliczki Péter Acsai Károly Bányász Tamás (1960-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus)
Internet cím:DOI
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