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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:BIBFORM020231
035-os BibID: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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3.

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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4.

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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5.

001-es BibID:BIBFORM049664
Első szerző:Magyar János (élettanász)
Cím:SEA0400 Fails To Alter The Magnitude Of Intracellular Ca2+ Transients And Contractions In Guinea Pig Heart / János Magyar, Norbert Szentandrássy, Péter Birinyi, Attila Farkas, András Tóth, László Csernoch, András Varró, Péter P. Nánási
Dátum:2009
ISSN:0006-3495
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
Megjelenés:Biophysical Journal. - 96 : 3 (2009), p. 512a. -
További szerzők:Szentandrássy Norbert (1976-) (élettanász) Birinyi Péter (1981-) (élettanász) Farkas Attila (1961-) (farmakológus) Tóth András (farmakológus) Csernoch László (1961-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
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6.

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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7.

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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8.

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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9.

001-es BibID:BIBFORM020356
Első szerző:Nagy N. (Szeged)
Cím:Role of Ca(2)+-sensitive K+ currents in controlling ventricular repolarization : possible implications for future antiarrhytmic drug therapy / Nagy N., Marton Z., Kiss L., Varro A., Nanasi P. P., Toth A.
Dátum:2011
ISSN:1875-533X (Electronic)
Megjegyzések:Normal heart function and repolarization of the cardiac action potential (AP) is to a high extent subjective to synchronized activity of sarcolemmal K(+) channels, expressed in both ventricular and atrial myocardium, largely contributing to regulation of the resting potential, the pacemaker activity, and the shape and duration of the AP. Clinical observations and experimental studies in cardiomyocytes and multicellular preparations provided firm evidence for the sensitivity of some major outward K+ currents and the corresponding ion channels to shifts in intracellular Ca(2+) concentration ([Ca(2+)](i)). Direct regulation via interaction between [Ca(2+ )](i) and the channel protein or indirect modulation via Ca(2+ ) signaling pathways of these currents have strong implications to mechanical and electrical performance of the heart, and its physiological adaptation to altered load. It may also lead to severe cardiac dysfunction, if [Ca(2+ )](i) handling is disturbed in a variety of pathological conditions. In this review we attempt to summarize the present state of the topic on two ubiquitous repolarizing K(+) currents (I(to1) and I(K1)) with documented Ca(2+)-sensitivity and critical significance in cellular antiarrhythmic defense, to highlight fields where clue data are missing, and discuss the apparently unsolved "mystery" of the cardiac small conductance Ca(2+ )-activated K(+ ) (SK) channels. We have collected the available information on the known novel, although usually still not enough selective inhibitors and activators of these currents justifying the need for more selective ones. Finally, we emphasize a few related therapeutical perspectives to be considered for future experimental research and particularly in pharmaceutical development.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Current Medicinal Chemistry. - 18 : 24 (2011), p. 3622-3639. -
További szerzők:Marton Z. Kiss L. Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász) Tóth András (farmakológus)
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10.

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)
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11.

001-es BibID:BIBFORM065571
Első szerző:Nánási Péter Pál (élettanász)
Cím:Power of the action potential voltage clamp technique / Péter P. Nánási, Norbert Szentandrássy, András Tóth, Tamás Bányász
Dátum:2009
Tárgyszavak:Orvostudományok Elméleti orvostudományok könyvfejezet
Megjelenés:Advances in Cardiomyocyte Research / Szerk. Nánási Péter P. - p. 93-119. -
További szerzők:Szentandrássy Norbert (1976-) (élettanász) Tóth András (farmakológus) Bányász Tamás (1960-) (élettanász)
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12.

001-es BibID:BIBFORM004111
Első szerző:Szentandrássy Norbert (élettanász)
Cím:SEA0400 fails to alter the magnitude of intracellular Ca2+ transients and contractions in Langendorff-perfused guinea pig hearts / Szentandrássy N., Birinyi P., Szigeti Gy., Farkas A., Magyar J., Tóth A., Csernoch L., Varró A., Nánási P.P.
Dátum:2008
Megjegyzések:SEA0400 is a recently developed inhibitor of the Na+/Ca2+ exchanger (NCX) shown to suppress both forward and reverse mode operation of NCX. Present experiments were designed to study the effect of partial blockade of NCX on Ca handling and contractility in Langendorff-perfused guinea pig hearts loaded with the fluorescent Ca-sensitive dye fura-2. Left ventricular pressure and intracellular calcium concentration ([Ca2+]i) were synchronously recorded before and after cumulative superfusion with 0.3 and 1 muM SEA0400. SEA0400 caused no significant change in the systolic and diastolic values of left ventricular pressure and [Ca2+]i. Accordingly, pulse pressure and amplitude of the [Ca2+]i transient also remained unchanged in the presence of SEA0400. SEA0400 had no influence either on the time required to reach peak values of pressure and [Ca2+)]i or on half relaxation time. On the other hand, both 0.3 and 1 microM SEA0400 significantly increased the decay time constant of [Ca2+]i transients, obtained by fitting its descending limb between 30% and 90% of relaxation, from 127 +/- 7 to 165 +/- 7 and 177 +/- 14 ms, respectively (P < 0.05, n=6). In contrast to the guinea pig hearts, rat hearts responded to SEA0400 treatment with increased [Ca2+]i transients and contractility. These interspecies differences observed in the effect of SEA0400 can be explained by the known differences in calcium handling between the two species.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Naunyn-Schmiedeberg's Archives of Pharmacology. - 378 : 1 (2008), p. 65-71. -
További szerzők:Birinyi Péter (1981-) (élettanász) Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Farkas Attila (1961-) (farmakológus) Magyar János (1961-) (élettanász) Tóth András (farmakológus) Csernoch László (1961-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
Internet cím:elektronikus változat
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