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1.

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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2.

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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3.

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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4.

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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5.

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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6.

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)
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7.

001-es BibID:BIBFORM037989
Első szerző:Bárándi László (élettanász)
Cím:A ropinirol elektrofiziológiai hatásai kutya kamrai szívizomsejteken / Bárándi László, Simkó József, Harmati Gábor, Bányász Tamás, Magyar János, Szentandrássy Norbert, Horváth Balázs, Nánási Péter Pál
Dátum:2010
Tárgyszavak:Orvostudományok Egészségtudományok idézhető absztrakt
Megjelenés:Cardiologia Hungarica. - 40 (2010), p. G34. -
További szerzők:Simkó József (1974-) (belgyógyász, kardiológus) Harmati Gábor (1983-) (élettanász) Bányász Tamás (1960-) (élettanász) Magyar János (1961-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Horváth Balázs (1981-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
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8.

001-es BibID:BIBFORM016887
Első szerző:Bárándi László (élettanász)
Cím:Drug-induced changes in action potential duration are proportional to action potential duration in rat ventricular myocardium / Bárándi, L., Harmati, G., Horváth, B., Szentandrássy, N., Magyar, J., Varró, A., Nánási, P.P., Bányász, T.
Dátum:2010
ISSN:0231-5882
Megjegyzések:Several cardioactive agents exhibit direct or reverse rate-dependent effects on action potential duration (APD) depending on the experimental conditions. Recently, a new theory has been proposed, suggesting that the reverse rate-dependent mode of drug-action may be a common property of canine, rabbit, guinea pig and human cardiac tissues, and this phenomenon is based on the dependence of drug-action on baseline APD. The aim of the present work was to examine the limitations of this hypothesis by studying the APD lengthening effect of K+ channel blockers and the APD shortening effect of Ca2+ channel blockers during the electrical restitution process of rat ventricular action potentials. Rat ventricular muscle was chosen because it has a set of ion currents markedly different from those of other species, its APD is shorter by one order of magnitude than that of the "plateau-forming" larger mammals, and most importantly, its APD increases at higher heart rates ? opposite to many other species. The restitution of APD was studied as a function of the diastolic interval, a parameter indicating the proximity of action potentials. It was found that drug-induced APD changes in rat myocardium are proportional with the pre-drug value of APD but not with the diastolic interval, indicating that not the proximity of consecutive action potentials, but the baseline APD itself may determine the magnitude of drug-induced APD changes.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Action potential duration
Electrical restitution
Membrane current
Reverse rate dependence
Ventricular repolarization
Megjelenés:General Physiology And Biophysics. - 29 : 3 (2010), p. 309-313. -
További szerzők:Harmati Gábor (1983-) (élettanász) Horváth Balázs (1981-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Magyar János (1961-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász) Bányász Tamás (1960-) (élettanász)
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9.

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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10.

001-es BibID:BIBFORM032923
035-os BibID:PMID:16086157
Első szerző:Birinyi Péter (élettanász)
Cím:Effects of SEA0400 and KB-R7943 on Na+/Ca2+ exchange current and L-type Ca2+ current in canine ventricular cardiomyocytes / Péter Birinyi, Károly Acsai, Tamás Bányász, András Tóth, Balázs Horváth, László Virág, Norbert Szentandrássy, János Magyar, András Varró, Ferenc Fülöp, Péter P. Nánási
Dátum:2005
ISSN:0028-1298
Megjegyzések:SEA0400 and KB-R7943 are compounds synthesised to block transsarcolemmal Na+/Ca2+ exchange current (INa/Ca); however, they Have also been shown to inhibit L-type Ca2+ current (ICa). The potential value of these compounds depends critically on their relative selectivity for INa/Ca over ICa. In the present work, therefore, the concentration-dependent effects of SEA0400 and KB-R7943 on INa/Ca and ICa were studied and compared in canine ventricular cardiomyocytes using the whole-cell configuration of the patch clamp technique. SEA0400 and KB-R7943 decreased INa/Ca in a concentration-dependent manner, having EC50 values of 111?43 nM and 3.35?0.82 mgrM, when suppressing inward currents, while the respective EC50 values were estimated at 108?18 nM and 4.74?0.69 mgrM in the case of outward current block. SEA0400 and KB-R7943 also blocked ICa, having comparable EC50 values (3.6 mgrM and 3.2 mgrM, respectively). At higher concentrations (10 mgrM) both drugs accelerated inactivation of ICa, retarded recovery from inactivation and shifted the voltage dependence of inactivation towards more negative voltages. The voltage dependence of activation was slightly modified by SEA0400, but not by KB-R7943. Based on the relatively good selectivity of submicromolar concentrations of SEA0400?but not KB-R7943?for INa/Ca over ICa, SEA0400 appears to be a suitable tool to study the role of INa/Ca in Ca2+ handling in canine cardiac cells. At concentrations higher than 1 mgrM, however, ICa is progressively suppressed by the compound.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
SEA0400
KB-R7943
Na+/Ca2+ exchanger
Ca2+ current
Cardiac cells
Dog
Voltage clamp
egyetemen (Magyarországon) készült közlemény
Megjelenés:Naunyn-Schmiedebergs Archives Of Pharmacology. - 372 : 1 (2005), p. 63-70. -
További szerzők:Acsai Károly Bányász Tamás (1960-) (élettanász) Tóth András Horváth Balázs (1981-) (élettanász) Virág László (élettanász Szeged) Szentandrássy Norbert (1976-) (élettanász) Magyar János (1961-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Fülöp Ferenc (Szeged) Nánási Péter Pál (1956-) (élettanász)
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11.

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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DOI
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12.

001-es BibID:BIBFORM099534
035-os BibID:(cikkazonosító)40 (Wos)000758039900001 (Scopus)85122159605
Első szerző:Dienes Csaba (gyógyszerész)
Cím:Pharmacological Modulation and (Patho)Physiological Roles of TRPM4 Channel-Part 2 : TRPM4 in Health and Disease / Csaba Dienes, Zsigmond Máté Kovács, Tamás Hézső, János Almássy, János Magyar, Tamás Bányász, Péter P. Nánási, Balázs Horváth, Norbert Szentandrássy
Dátum:2022
ISSN:1424-8247
Megjegyzések:Transient receptor potential melastatin 4 (TRPM4) is a unique member of the TRPM protein family and, similarly to TRPM5, is Ca2+ sensitive and permeable for monovalent but not divalent cations. It is widely expressed in many organs and is involved in several functions; it regulates membrane potential and Ca2+ homeostasis in both excitable and non-excitable cells. This part of the review discusses the currently available knowledge about the physiological and pathophysiological roles of TRPM4 in various tissues. These include the physiological functions of TRPM4 in the cells of the Langerhans islets of the pancreas, in various immune functions, in the regulation of vascular tone, in respiratory and other neuronal activities, in chemosensation, and in renal and cardiac physiology. TRPM4 contributes to pathological conditions such as overactive bladder, endothelial dysfunction, various types of malignant diseases and central nervous system conditions including stroke and injuries as well as in cardiac conditions such as arrhythmias, hypertrophy, and ischemia-reperfusion injuries. TRPM4 claims more and more attention and is likely to be the topic of research in the future.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
TRPM4
SUR1
pancreatic beta-cell
cancer
neuronal
immune system
urinary bladder
cardiac
vascular tone
central nervous system injury
Megjelenés:Pharmaceuticals. - 15 : 1 (2022), p. 40. -
További szerzők:Kovács Zsigmond Máté (1995-) (orvos) Hézső Tamás (1993-) (élettanász) Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Horváth Balázs (1981-) (élettanász) Szentandrássy Norbert (1976-) (élettanász)
Pályázati támogatás:FK-128116
OTKA
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