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1.

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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2.

001-es BibID:BIBFORM096079
035-os BibID:(cikkazonosító)9565 (WOS)000656453000010 (Scopus)85105210158
Első szerző:Hézső Tamás (élettanász)
Cím:Mexiletine-like cellular electrophysiological effects of GS967 in canine ventricular myocardium / Tamás Hézső, Muhammad Naveed, Csaba Dienes, Dénes Kiss, János Prorok, Tamás Árpádffy-Lovas, Richárd Varga, Erika Fujii, Tanju Mercan, Leila Topal, Kornél Kistamás, Norbert Szentandrássy, János Almássy, Norbert Jost, János Magyar, Tamás Bányász, István Baczkó, András Varró, Péter P. Nánási, László Virág, Balázs Horváth
Dátum:2021
ISSN:2045-2322
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Scientific Reports. - 11 (2021), p. 9565. -
További szerzők:Naveed, Muhammad Dienes Csaba (1995-) (gyógyszerész) Kiss Dénes Zsolt (1995-) (orvos, élettanász) Prorok János Árpádffy-Lovas Tamás Varga Richárd Fujii Erika Mercan, Tanju Topal Leila Kistamás Kornél (1986-) (biológus) Szentandrássy Norbert (1976-) (élettanász) Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Jost Norbert Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Baczkó István Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász) Virág László (élettanász Szeged) Horváth Balázs (1981-) (élettanász)
Pályázati támogatás:FK128116
OTKA
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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: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:BIBFORM009061
Első szerző:Jost Norbert
Cím:Contribution of I Kr and I K1 to ventricular repolarization in canine and human myocytes : is there any influence of action potential duration? / Jost, N., Acsai, K., Horvath, B., Banyasz, T., Baczko, I., Bitay, M., Bogats, G., Nanasi, P. P.
Dátum:2009
ISSN:0300-8428 (Print)
Megjegyzések:The aim of the present work was to study the profile of the rapid delayed rectifier potassium current (I (Kr)) and the inward rectifier potassium current (I (K1)) during ventricular repolarization as a function of action potential duration and rate of repolarization. METHODS: Whole cell configuration of the patch clamp technique was used to monitor I (Kr) and I (K1) during the action potential plateau and terminal repolarization. Action potentials recorded at various cycle lengths (0.4-5 s) and repolarizing voltage ramps having various slopes (0.5-3 V/s) were used as command signals. I (Kr) and I (K1) were identified as difference currents dissected by E-4031 and BaCl(2), respectively. RESULTS: Neither peak amplitudes nor mean values of I (Kr) and I (K1) recorded during the plateau of canine action potentials were influenced by action potential duration. The membrane potential where I (Kr) and I (K1) peaked during the terminal repolarization was also independent of action potential duration. Similar results were obtained in undiseased human ventricular myocytes, and also in canine cells when I (Kr) and I (K1) were evoked using repolarizing voltage ramps of various slopes. Action potential voltage clamp experiments revealed that the peak values of I (Kr), I (K1), and net outward current during the terminal repolarization were independent of the pacing cycle length within the range of 0.4 and 5 s. CONCLUSIONS: The results indicate that action potential configuration fails to influence the amplitude of I (Kr) and I (K1) during the ventricular action potential in dogs and humans, suggesting that rate-dependent changes in action potential duration are not likely related to rate-dependent alterations in I (Kr) or I (K1) kinetics in these species.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Action Potentials
Animals
Barium Compounds
Chlorides
Dogs
Electrophysiology
Humans
KATP Channels
Kinetics
Muscle Cells
Patch-Clamp Techniques
Potassium Channels, Inwardly Rectifying
Reference Values
Ventricular Function
Megjelenés:Basic Research in Cardiology. - 104 : 1 (2009), p. 33-41. -
További szerzők:Acsai Károly Horváth Balázs (1981-) (élettanász) Bányász Tamás (1960-) (élettanász) Baczkó István Bitay Miklós Bogáts Gábor Nánási Péter Pál (1956-) (élettanász)
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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: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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8.

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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Borító:

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:BIBFORM095978
035-os BibID:(WoS)000690082000001 (Scopus)85112668920
Első szerző:Nánási Péter Pál (élettanász)
Cím:Canine Myocytes Represent a Good Model for Human Ventricular Cells Regarding Their Electrophysiological Properties / Péter P. Nánási, Balázs Horváth, Fábián Tar, János Almássy, Norbert Szentandrássy, Norbert Jost, István Baczkó, Tamás Bányász, András Varró
Dátum:2021
ISSN:1424-8247
Megjegyzések:Due to the limited availability of healthy human ventricular tissues, the most suitable animal model has to be applied for electrophysiological and pharmacological studies. This can be best identified by studying the properties of ion currents shaping the action potential in the frequently used laboratory animals, such as dogs, rabbits, guinea pigs, or rats, and comparing them to those of human cardiomyocytes. The authors of this article with the experience of three decades of electrophysiological studies, performed in mammalian and human ventricular tissues and isolated cardiomyocytes, summarize their results obtained regarding the major canine and human cardiac ion currents. Accordingly, L-type Ca2+ current (ICa), late Na+ current (INa-late), rapid and slow components of the delayed rectifier K+ current (IKr and IKs, respectively), inward rectifier K+ current (IK1), transient outward K+ current (Ito1), and Na+/Ca2+ exchange current (INCX) were characterized and compared. Importantly, many of these measurements were performed using the action potential voltage clamp technique allowing for visualization of the actual current profiles flowing during the ventricular action potential. Densities and shapes of these ion currents, as well as the action potential configuration, were similar in human and canine ventricular cells, except for the density of IK1 and the recovery kinetics of Ito. IK1 displayed a largely four-fold larger density in canine than human myocytes, and Ito recovery from inactivation displayed a somewhat different time course in the two species. On the basis of these results, it is concluded that canine ventricular cells represent a reasonably good model for human myocytes for electrophysiological studies, however, it must be borne in mind that due to their stronger IK1, the repolarization reserve is more pronounced in canine cells, and moderate differences in the frequency-dependent repolarization patterns can also be anticipated.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
cardiac ion currents
human ventricular cells
canine myocytes
action potential configuration
action potential voltage clamp
Megjelenés:Pharmaceuticals. - 14 : 8 (2021), p. 748. -
További szerzők:Horváth Balázs (1981-) (élettanász) Tar Fábián Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Szentandrássy Norbert (1976-) (élettanász) Jost Norbert Baczkó István Bányász Tamás (1960-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus)
Pályázati támogatás:FK128116
OTKA
NKFIH K-119992
OTKA
NKFIH-PD120794
OTKA
NKFIH-FK128116
OTKA
K-135464
OTKA
K-128851
OTKA
TKP2020-NKA-04
Egyéb
ED-18-1-2019-0028
Egyéb
20391-3/2018/FEKUSTRAT
Egyéb
GINOP-2.3.2-15-2016-00040
GINOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

11.

001-es BibID:BIBFORM082084
035-os BibID:(WoS)000582745400009 (Scopus)85075368709 (PubMed)31726065
Első szerző:Nánási Péter Pál (élettanász)
Cím:Implication of frequency-dependent protocols in antiarrhythmic and proarrhythmic drug testing / Péter P. Nánási, Zoltán Szabó, Kornél Kistamás, Balázs Horváth, László Virág, Norbert Jost, Tamás Bányász, János Almássy, András Varró
Dátum:2020
ISSN:0079-6107
Megjegyzések:It has long been known that the electrophysiological effects of many cardioactive drugs strongly depend on the rate dependent frequency. This was recognized first for class I antiarrhythmic agents: their Vmax suppressive effect was attenuated at long cycle lengths. Later many Ca2+ channel blockers were also found to follow such kinetics. The explanation was provided by the modulated and the guarded receptor theories. Regarding the duration of cardiac action potentials (APD) an opposite frequency-dependence was observed, i.e. the drug-induced changes in APD were proportional with the cycle length of stimulation, therefore it was referred as "reverse rate-dependency". The beat-to-beat, or short term variability of APD (SV) has been recognized as an important proarrhythmic mechanism, its magnitude can be used as an arrhythmia predictor. SV is modulated by several cardioactive agents, however, these drugs modify also APD itself. In order to clear the drug-specific effects on SV from the concomitant unspecific APD-change related ones, the term of "relative variability" was introduced. Relative variability is increased by ion channel blockers that decrease the negative feedback control of APD (i.e. blockers of ICa, IKr and IKs) and also by elevation of cytosolic Ca2+. Cardiac arrhythmias are also often categorized according to the characteristic heart rate (tachy- and bradyarrhythmias). Tachycardia is proarrhythmic primarily due to the concomitant Ca2+ overload causing delayed afterdepolarizations. Early afterdepolarizations (EADs) are complications of the bradycardic heart. What is common in the reverse rate-dependent nature of drug action on APD, increased SV and EAD incidence associated with bradycardia.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Cardiac myocytes
Cardiac arrhythmias
Action potential duration
Cardiac ion currents
Rate-dependent actions
Reverse rate-dependency
Short term variability
Triggered activity
Megjelenés:Progress In Biophysics & Molecular Biology. - 157 (2020), p. 76-83. -
További szerzők:Szabó Zoltán (1973-) (belgyógyász, kardiológus) Kistamás Kornél (1986-) (biológus) Horváth Balázs (1981-) (élettanász) Virág László (élettanász Szeged) Jost Norbert Bányász Tamás (1960-) (élettanász) Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Varró András (1954-) (farmakológus, klinikai farmakológus)
Pályázati támogatás:NKFIH K115397
egyéb
NKFIH K-119992
egyéb
GINOP-2.3.2.-15-2016-00040
GINOP
20391-3/2018/FEKUSTRAT
egyéb
EFOP-3.6.2-16-2017-00006
EFOP
ED_18-1-2019-0028
egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

12.

001-es BibID:BIBFORM114227
035-os BibID:(cikkazonosító)2383 (WoS)001075914200001 (Scopus)85172453453
Első szerző:Naveed, Muhammad
Cím:Selective Inhibition of Cardiac Late Na+ Current Is Based on Fast Offset Kinetics of the Inhibitor / Naveed Muhammad, Mohammed Aiman Saleh A., Topal Leila, Kovács Zsigmond Máté, Dienes Csaba, Ovári József, Szentandrássy Norbert, Magyar János, Bányász Tamás, Prorok János, Jost Norbert, Virág László, Baczkó István, Varró András, Nánási Péter P., Horváth Balázs
Dátum:2023
ISSN:2227-9059
Megjegyzések:The present study was designed to test the hypothesis that the selectivity of blocking the late Na+ current (I-NaL) over the peak Na+ current (I-NaP) is related to the fast offset kinetics of the Na+ channel inhibitor. Therefore, the effects of 1 mu M GS967 (I-NaL inhibitor), 20 mu M mexiletine (I/B antiarrhythmic) and 10 mu M quinidine (I/A antiarrhythmic) on I-NaL and I-NaP were compared in canine ventricular myocardium. I-NaP was estimated as the maximum velocity of action potential upstroke (V-max(+)). Equal amounts of I-NaL were dissected by the applied drug concentrations under APVC conditions. The inhibition of I-NaL by mexiletine and quinidine was comparable under a conventional voltage clamp, while both were smaller than the inhibitory effect of GS967. Under steady-state conditions, the V-max(+) block at the physiological cycle length of 700 ms was 2.3% for GS967, 11.4% for mexiletine and 26.2% for quinidine. The respective offset time constants were 110 +/- 6 ms, 456 +/- 284 ms and 7.2 +/- 0.9 s. These results reveal an inverse relationship between the offset time constant and the selectivity of I-NaL over I-NaP inhibition without any influence of the onset rate constant. It is concluded that the selective inhibition of I-NaL over I-NaP is related to the fast offset kinetics of the Na+ channel inhibitor.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
late Na+ current
class I antiarrhythmics
rate-dependent block
dog myocytes
GS967
Megjelenés:Biomedicines. - 11 : 9 (2023), p. 2383. -
További szerzők:Mohammed, Aiman Saleh A. Topal Leila Kovács Zsigmond Máté (1995-) (orvos) Dienes Csaba (1995-) (gyógyszerész) Óvári József (1997-) (PhD hallgató) Szentandrássy Norbert (1976-) (élettanász) Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Prorok János Jost Norbert Virág László (élettanász Szeged) Baczkó István Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász) Horváth Balázs (1981-) (élettanász)
Pályázati támogatás:NKFIH-K138090
Egyéb
NKFIH-K142764
Egyéb
NKFIH-FK128116
Egyéb
NKFIH K142738
Egyéb
NKFIH K128851
Egyéb
GINOP-2.3.2-15-2016-00048
GINOP
EFOP-3.6.2-16-2017-00006
EFOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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