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1.

001-es BibID:BIBFORM120412
035-os BibID:(WoS)000089378200115
Első szerző:Bányász Tamás (élettanász)
Cím:Inhibitory role of chloride current on delayed after-depolarization in canine ventricular myocytes / Bányász T., Magyar J., Nánási P. P.
Dátum:2000
ISSN:0022-3751 1469-7793
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Journal Of Physiology-London. - 526 : suppl (2000), p. 81P. -
További szerzők:Magyar János (1961-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
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2.

001-es BibID:BIBFORM055068
Első szerző:Bányász Tamás (élettanász)
Cím:An emerging antiarrhythmic target : late sodium current / Banyasz T., Szentandrássy N., Magyar J., Szabo Z., Nánási P. P., Chen-Izu Y., Izu L. T.
Dátum:2015
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Current Pharmacological Design. - 21 : 8 (2015), pp. 1073-1090. -
További szerzők:Szentandrássy Norbert (1976-) (élettanász) Magyar János (1961-) (élettanász) Szabó Zoltán (1973-) (belgyógyász, kardiológus) Nánási Péter Pál (1956-) (élettanász) Chen-Izu, Ye Izu, Leighton T.
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3.

001-es BibID:BIBFORM044406
035-os BibID:(dekdb)bibKLT00081800
Első szerző:Bányász Tamás (élettanász)
Cím:Exercise book : a physiology laboratory guide / Tamás Bányász, Julianna Cseri, László Csernoch, Miklós Dankó, István Jóna, László Kónya, Péter Nánási
Dátum:1994
Megjelenés:Debrecen : University Medical School of Debrecen, 1994
Terjedelem:105 p.
Tárgyszavak:Orvostudományok Elméleti orvostudományok feladatgyűjtemény
Élettan
További szerzők:Cseri Julianna (1949-2022) (laboratóriumi diagnosztika szakorvos) Csernoch László (1961-) (élettanász) Dankó Miklós Jóna István (1948-) (élettanász, fizikus) Kónya László Nánási Péter Pál (1956-) (élettanász)
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4.

001-es BibID:BIBFORM037025
Első szerző:Bányász Tamás (élettanász)
Cím:Reverse rate dependency is an intrinsic property of canine cardiac preparations / Banyasz Tamas, Horvath Balazs, Virag Laszlo, Barandi Laszlo, Szentandrassy Norbert, Harmati Gabor, Magyar Janos, Marangoni Stefano, Zaza Antonio, Varro Andras, Nanasi Peter P.
Dátum:2009
ISSN:0008-6363
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 reverse rate-dependent drug effects. Methods and resultsAction potentials were recorded from multicellular canine ventricular preparations and isolated cardiomyocytes, at cycle lengths (CLs) varying from 0.3 to 5 s, using conventional sharp microelectrodes. APD was either modified by applying inward and outward current pulses, or by superfusion of agents known to lengthen and shorten APD. Net membrane current (Im) was calculated from action potential waveforms. The hypothesis that RRD may be implicit in the relationship between Im and APD was tested by numerical modelling. Both drug-induced lengthening (by veratrine, BAY-K 8644, dofetilide, and BaCl2) and shortening (by lidocaine and nicorandil) of action potentials displayed RRD, i.e. changes in APD were greater at longer than at shorter CL. A similar dependency of effect on CL was found when repolarization was modified by injection of inward or outward current pulses. Im measured at various points during repolarization was inversely proportional to APD and to CL. Model simulations showed that RRD is expected as a consequence of the non-linearity of the relationship between Im and APD. ConclusionRRD of APD modulation is shared, although with differences in magnitude, by interventions of very different nature. RRD can be interpreted as a consequence of the relationship between Im and APD and, as such, is expected in all species having positive APD-CL relationship. This implies that the development of agents prolonging APD with direct rate dependency, or even completely devoid of RRD, may be difficult to achieve.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Cardiovascular Research. - 84 : 2 (2009), p. 237-244. -
További szerzők:Horváth Balázs (1981-) (élettanász) Virág László (élettanász Szeged) Bárándi László (1984-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Harmati Gábor (1983-) (élettanász) Magyar János (1961-) (élettanász) Marangoni, Stefano Zaza, Antonio Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
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5.

001-es BibID:BIBFORM032954
Első szerző:Bányász Tamás (élettanász)
Cím:Frequency-dependent characteristics of human cardiac muscle / Tamás Bányász, János Magyar, Péter Szigligeti, Csaba Pankucsi, András Varró, Péter P. Nánási
Dátum:1997
Megjegyzések:OBJECTIVES: To characterize the steady state frequency-dependent properties and restitution kinetics of action potential duration (APD) in isolated human atrial and ventricular cardiac muscle preparations. MATERIALS AND METHODS: Conventional microelectrode techniques were used to record action potentials in preparations of human left ventricular muscle and right atrial appendages under steady state conditions or after abrupt changes in cycle length, ie, following increasingly longer diastolic intervals (DI). Restitution relations were generated by plotting APD against the respective DI. Restitution relations were fitted to multiexponential functions. RESULTS: Restitution of APD at 90% repolarization in ventricular preparations, paced at a basic cycle length (BCL) of 750 ms, were fitted as the sum of four exponentials, having time constants of 42.8 ms, 139 ms, 1.34 s and 16 s. Similar results were obtained for restitution of values of APD at 50% repolarization. In atrial preparations, restitution kinetics were characterized by three exponentials with time constants of 154 ms, 1.52 s and 25.5 s (BCL of 750 ms). The very fast component of restitution, observed in ventricular muscle, was apparently missing in atrial fibres. When atrial preparations were paced at a longer BCL of 5000 ms, no change in time constants of restitution was observed; however, the amplitudes of the second and third atrial components decreased significantly compared with preparations paced at a BCL of 750 ms. CONCLUSIONS: Comparing the time constant values estimated for restitution with the reported kinetic parameters of cardiac ion channels, it may be speculated that the first component of restitution in ventricular muscle is attributed to the recovery of L-type calcium current from inactivation. The lack of this very rapid component in atrial muscle can be explained by the parallel recovery of the calcium current and the transient outward potassium current, prominent in atrial myocardium. The second ventricular component (first in atrium) may be due to the time-dependent deactivation of the delayed rectifier potassium current. The third and fourth ventricular components (second and third components, respectively, in the atrium) are probably related to transient changes in intracellular ionic composition.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Experimental And Clinical Cardiology 2 : 3 (1997), p. 205-209. -
További szerzők:Magyar János (1961-) (élettanász) Szigligeti Péter Pankucsi Csaba (farmakológus) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
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6.

001-es BibID:BIBFORM030274
035-os BibID:WOS:000079560700007
Első szerző:Bányász Tamás (élettanász)
Cím:EGIS-7229, the new combined class III antiarrhythmic agent : lack of EAD inducing effect / Tamás Bányász, János Magyar, András Varró, Anikó Kovács, Ildikó Gyönös, Gábor Szénási, Péter P. Nánási
Dátum:1999
ISSN:0306-3623
Megjegyzések:EGIS-7229 is a novel antiarrhythmic candidate having multiple mechanisms of action with class III predominance. In this study, the effects of EGIS-7229 and sotalol on action potential duration (APD) and incidence of early afterdepolarizations (EADs) were studied and compared in rabbit papillary muscle by using conventional microelectrode techniques. In control bathing solution, both drugs increased APD in a concentration-dependent manner; however, the prolongation of APD was greater with sotalol than with EGIS-7229 when the same drug concentrations were compared. EAD developed in 3 of the 11 preparations (27%) bathed with a solution containing 3.6 mmol/l CsCl + 2 mmol/l KCl within the first 120 min of superfusion. The addition of 100 mu mol/l sotalol to this superfusate increased the incidence of EAD to 83% (10 from 12), whereas the addition of the same concentration of EGIS-7229 prevented the development of EAD in all of the 9 preparations studied. These differences in incidence of EAD are likely attributable to differences in drug-induced increases of APD-50 in the presence of CsCl. Prolongation of APD-90 showed less correlation with incidence of EAD than changes in APD-50. On the basis of these in vitro results, high concentrations of EGIS-7229 cannot be expected to be torsadogenic in vivo-in contrast with sotalol-presumably owing to the combined class III + IV activity of the compound. (C) 1999 Elsevier Science Inc. All rights reserved.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:General Pharmacology. - 32 : 3 (1999), p. 329-333. -
További szerzők:Magyar János (1961-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Kovács Anikó Gyönös Ildikó Szénási Gábor Nánási Péter Pál (1956-) (élettanász)
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7.

001-es BibID:BIBFORM030253
Első szerző:Bányász Tamás (élettanász)
Cím:Different effects of endothelin-1 on calcium and potassium currents in canine ventricular cells / Tamás Bányász, János Magyar, Ágnes Körtvély, Gyula Szigeti, Péter Szigligeti, Zoltán Papp, Attila Mohácsi, László Kovács, Péter P. Nánási
Dátum:2001
ISSN:0028-1298
Megjegyzések:Effects of endothelin-l (ET-1) on the L-type calcium current (I-Ca) and delayed rectifier potassium current (I-K) were studied in isolated canine ventricular cardiomyocytes using the whole-cell configuration of the patch-clamp technique. ET-1 (8 nM) was applied in three experimental arrangements: untreated cells, in the presence of 50 nM isoproterenol, and in the presence of 250 muM 8-bromo-cAMP. In untreated cells, ET-1 significantly decreased the peak amplitude of I-Ca by 32.3 +/-4.8% at +5 mV (P<0.05) without changing activation or inactivation characteristics of I-Ca. ET-1 had no effect on the amplitude of I-K, I-to (transient outward current) or I-K1 (inward rectifier K current) in untreated cells; however, the time course of recovery from inactivation of I-to was significantly increased by ET-1 (from 26.5<plus/minus>6 ms to 59.5 +/- 1.8 ms, P<0.05). Amplitude and time course of intracellular calcium transients, recorded in voltage-clamped cells previously loaded with the fluorescent calcium indicator dye Fura-2, were not affected by ET-1. ET-1 had no effect on force of contraction in canine ventricular trabeculae. Isoproterenol increased the amplitude of I-Ca to 263<plus/minus> 29% of control. ET-1 reduced I-Ca also in isoproterenol-treated cells by 17.8 +/-2% (P<0.05); this inhibition was significantly less than obtained in untreated cells. I-K was increased by isoproterenol to 213<plus/minus>18% of control. This effect of isoproterenol on I-K was reduced by 31.8 +/-4.8% if the cells were pretreated with ET-1. Similarly, in isoproterenol-treated cells ET-1 decreased I-K by 16.2 +/-1.5% (P<0.05). Maximal activation of protein kinase A (PKA) was achieved by application of 8-bromo-cAMP in the pipette solution. In the presence of 8-bromo-cAMP ET-l failed to alter I-CA or I-K It was concluded that differences in effects of ET-1 on I-CA and I-K may be related to differences in cAMP sensitivity of the currents.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Naunyn-Schmiedebergs Archives of Pharmacology. - 363 : 4 (2001), p. 383-390. -
További szerzők:Magyar János (1961-) (élettanász) Körtvély Ágnes Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Szigligeti Péter Papp Zoltán (1965-) (kardiológus, élettanász) Mohácsi Attila (1960-) (orvos) Kovács László (1939-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
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8.

001-es BibID:BIBFORM030251
035-os BibID:WOS:000182446700007
Első szerző:Bányász Tamás (élettanász)
Cím:Endocardial versus epicardial differences in L-type calcium current in canine ventricular myocytes studied by action potential voltage clamp / Tamás Bányász, László Fülöp, János Magyar, Norbert Szentandrássy, András Varró, Péter P. Nánási
Dátum:2003
ISSN:0008-6363
Megjegyzések:Objectives: The aim of the present study was to assess and compare the dynamics of L-type Ca2+ current (I-Ca.L) during physiologic action potential (AP) in canine ventricular cardiomyocytes of epicardial (EPI) and endocardial (ENDO) origin. Methods: I-Ca.L was recorded on cells derived from the two regions of the heart using both AP voltage clamp and conventional whole cell voltage clamp techniques. Results: AP voltage clamp experiments revealed that the decay of I-Ca.L is monotonic during endocardial AP, whereas the current is double-peaked (displaying a second rise) during epicardial AP. The amplitude of the first peak was significantly greater in ENDO (-4.6+/-0.8 pA/pF) than in EPI cells (-2.8+/-0.3 pA/pF). Application of epicardial APs as command pulses to endocardial cells yielded double-peaked I-Ca.L profiles, and increased the net charge entry carried by I-Ca.L during the AP from 0.187+/-0.059 to 0.262+/-0.056 pC/pF (n=5, P<0.05). No differences were observed in current densities and inactivation kinetics of I-Ca.L between EPI and ENDO cells when studied under conventional voltage clamp conditions. Nisoldipine shortened action potentials and eliminated the dome of the epicardial AP. Conclusion: I-Ca.L was shown to partially inactivate before and deactivate during phase-1 repolarization and reopening of these channels is responsible for the formation of the dome in canine EPI cells. The transmural differences in the profile of I-Ca.L could be well explained with differences in AP configuration. (C) 2003 European Society of Cardiology. Published by Elsevier Science B.V. All rights reserved.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Cardiovascular Research. - 58 : 1 (2003), p. 66-75. -
További szerzők:Fülöp László (1976-) (kardiológus) Magyar János (1961-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
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9.

001-es BibID:BIBFORM030249
035-os BibID:WOS:000187895800005
Első szerző:Bányász Tamás (élettanász)
Cím:Profile of I(Ks) during the action potential questions the therapeutic value of I(Ks) blockade / Tamás Bányász, Roland Koncz, László Fülöp, Norbert Szentandrássy, János Magyar, Péter P. Nánási
Dátum:2004
ISSN:0929-8673
Megjegyzések:The goal of this paper is two fold. First, we attempt to review the reports available on the role Of I-Ks in myocardial repolarization. Based on theoretical considerations and experimental results, it seems reasonable to assume that I-Ks blockade will lengthen the action potential. However, results obtained with I-Ks blockers, like chromanol 293B or L-735,821, are conflicting, since from slight lengthening to marked prolongation of action potentials were equally obtained. Although these contradictory results were explained by interspecies or regional differences, the role Of I-Ks in repolarization is a matter of growing dispute. In the second part of this study, we simulated the performance Of I-Ks during cardiac action potentials. We compared the profile of the predicted current in three mathematical models in order to determine the relative role of the current in repolarization. We studied the effect of the cycle length, action potential duration and height of the plateau on the profile Of I-Ks in epicardiac, endocardiac and midmyocardiac ventricular action potentials. The results indicate that the height of the plateau is the most important parameter to control activation Of I-Ks in cardiac tissues, and accordingly, the interspecies and regional differences observed in the efficacy Of I-Ks blockers are likely due to the known differences in action potential morphology. We conclude also that I-Ks blockade may have unpredictable effects on the length of the action potential in a diseased heart, questioning the possible therapeutic value of drugs blocking I-Ks.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Current Medicinal Chemistry. - 11 : 1 (2004), p. 45-60. -
További szerzők:Koncz Roland Fülöp László (1976-) (kardiológus) Szentandrássy Norbert (1976-) (élettanász) Magyar János (1961-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
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10.

001-es BibID:BIBFORM020231
035-os BibID:(Scopus)79551587546 (WoS)000294414700009
Első szerző:Bányász Tamás (élettanász)
Cím:Cardiac calmodulin kinase : a potential target for drug design / Banyasz T., Szentandrassy N., Toth A., Nanasi P. P., Magyar J., Chen-Izu Y.
Dátum:2011
ISSN:0929-8673
Megjegyzések:Therapeutic strategy for cardiac arrhythmias has undergone a remarkable change during the last decades. Currently implantable cardioverter defibrillator therapy is considered to be the most effective therapeutic method to treat malignant arrhythmias. Some even argue that there is no room for antiarrhythmic drug therapy in the age of implantable cardioverter defibrillators. However, in clinical practice, antiarrhythmic drug therapies are frequently needed, because implantable cardioverter defibrillators are not effective in certain types of arrhythmias (i.e. premature ventricular beats or atrial fibrillation). Furthermore, given the staggering cost of device therapy, it is economically imperative to develop alternative effective treatments. Cardiac ion channels are the target of a number of current treatment strategies, but therapies based on ion channel blockers only resulted in moderate success. Furthermore, these drugs are associated with an increased risk of proarrhythmia, systemic toxicity, and increased defibrillation threshold. In many cases, certain ion channel blockers were found to increase mortality. Other drug classes such as beta-blockers, angiotensin-converting enzyme inhibitors, aldosterone antagonists, and statins appear to have proven efficacy for reducing cardiac mortality. These facts forced researchers to shift the focus of their research to molecular targets that act upstream of ion channels. One of these potential targets is calcium/calmodulin-dependent kinase II (CaMKII). Several lines of evidence converge to suggest that CaMKII inhibition may provide an effective treatment strategy for heart diseases. (1) Recent studies have elucidated that CaMKII plays a key role in modulating cardiac function and regulating hypertrophy development. (2) CaMKII activity has been found elevated in the failing hearts from human patients and animal models. (3) Inhibition of CaMKII activity has been shown to mitigate hypertrophy, prevent functional remodeling and reduce arrhythmogenic activity. In this review, we will discuss the structural and functional properties of CaMKII, the modes of its activation and the functional consequences of CaMKII activity on ion channels.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Current Medicinal Chemistry. - 18 : 24 (2011), p. 3707-3713. -
További szerzők:Szentandrássy Norbert (1976-) (élettanász) Tóth András (farmakológus) Nánási Péter Pál (1956-) (élettanász) Magyar János (1961-) (élettanász) Chen-Izu, Ye
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11.

001-es BibID:BIBFORM024502
035-os BibID:(WoS)000294414700002 (Scopus)80052005781
Első szerző:Bányász Tamás (élettanász)
Cím:Mechanism of reverse rate-dependent action of cardioactive agents / Tamás Bányász, László Bárándi, Gábor Harmati, László Virág, Norbert Szentandrássy, Ildikó Márton, Antonio Zaza, András Varró, Péter P. Nánási
Dátum:2011
ISSN:0929-8673 1875-533X
Megjegyzések:Class 3 antiarrhythmic agents exhibit reverse rate-dependent lengthening of the action potential duration (APD), i.e. changes in APD are greater at longer than at shorter cycle lengths. In spite of the several theories developed to explain this reverse rate-dependency, its mechanism has been clarified only recently. The aim of the present study is to elucidate the mechanisms responsible for reverse rate-dependency in mammalian ventricular myocardium. Action potentials were recorded using conventional sharp microelectrodes from human, canine, rabbit, guinea pig, and rat ventricular myocardium in a rate-dependent manner. Rate-dependent drug-effects of various origin were studied using agents known to lengthen or shorten action potentials allowing thus to determine the drug-induced changes in APD as a function of the cycle length. Both drug-induced lengthening and shortening of action potentials displayed reverse rate-dependency in human, canine, and guinea pig preparations, but not in rabbit and rat myocardium. Similar results were obtained when repolarization was modified by injection of inward or outward current pulses in isolated canine cardiomyocytes. In contrast to reverse rate-dependence, drug-induced changes in APD well correlated with baseline APD values (i.e. that measured before the superfusion of drug or injection of current) in all of the preparations studied. Since the net membrane current (I(net)), determined from the action potential waveform at the middle of the plateau, was inversely proportional to APD, and consequently to cycle length, it is concluded that that reverse rate-dependency may simply reflect the inverse relationship linking I(net) to APD. In summary, reverse rate-dependency is an intrinsic property of drug action in the hearts of species showing positive APD - cycle length relationship, including humans. This implies that development of a pure K(+) channel blocking agent without reverse rate-dependent effects is not likely to be successful.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
antiarrhythmiás szerek
APD
Molekuláris Medicina
egyetemen (Magyarországon) készült közlemény
Megjelenés:Current medicinal chemistry. - 18 : 24 (2011), p. 3597-3606. -
További szerzők:Bárándi László (1984-) (élettanász) Harmati Gábor (1983-) (élettanász) Virág László (élettanász Szeged) Szentandrássy Norbert (1976-) (élettanász) Márton Ildikó (1954-) (fogszakorvos) Zaza, Antonio Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
A feszültségfüggő K-csatornák szerepe excitábilis sejtekben
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12.

001-es BibID:BIBFORM001011
Első szerző:Bányász Tamás (élettanász)
Cím:Action potencial clamp fingerprints of K+ currents in canine cardiomyocytes : their role in ventricular repolarization / Bányász T., Magyar J., Szentandrássy N., Horváth B., Birinyi P., Szentmiklósi J., Nánási P.
Dátum:2007
Megjegyzések:The aim of the present study was to give a parametric description of the most important K(+) currents flowing during canine ventricular action potential. METHODS: Inward rectifier K(+) current (I(K1)), rapid delayed rectifier K(+) current (I(Kr)), and transient outward K(+) current (I(to)) were dissected under action potential clamp conditions using BaCl(2), E-4031, and 4-aminopyridine, respectively. RESULTS: The maximum amplitude of I(to) was 3.0 +/- 0.23 pA/pF and its integral was 29.7 +/- 2.5 fC/pF. The current peaked 4.4 +/- 0.7 ms after the action potential upstroke and rapidly decayed to zero with a time constant of 7.4 +/- 0.6 ms. I(Kr) gradually increased during the plateau, peaked 7 ms before the time of maximum rate of repolarization (V(max)(-)) at -54.2 +/- 1.7 mV, had peak amplitude of 0.62 +/- 0.08 pA/pF, and integral of 57.6 +/- 6.7 fC/pF. I(K1) began to rise from -22.4 +/- 0.8 mV, peaked 1 ms after the time of V(max)(-) at -58.3 +/- 0.6 mV, had peak amplitude of 1.8 +/- 0.1 pA/pF, and integral of 61.6 +/- 6.2 fC/pF. Good correlation was observed between peak I(K1) and V(max)(-) (r = 0.93) but none between I(Kr) and V(max)(-). Neither I(K1) nor I(Kr) was frequency-dependent between 0.2 and 1.66 Hz. Congruently, I(Kr) failed to accumulate in canine myocytes at fast driving rates. CONCLUSION: Terminal repolarization is dominated by I(K1), but action potential duration is influenced by several ion currents simultaneously. As I(to) was not active during the plateau, and neither I(K1) nor I(Kr) was frequency-dependent, other currents must be responsible for the frequency dependence of action potential duration at normal and slow heart rates in canine ventricular cells.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Acta Physiologica (Oxford, England). - 190 : 3 (2007), p. 189-198. -
További szerzők:Magyar János (1961-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Horváth Balázs (1981-) (élettanász) Birinyi Péter (1981-) (élettanász) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Nánási Péter Pál (1956-) (élettanász)
Internet cím:elektronikus változat
DOI
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