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1.

001-es BibID:BIBFORM074550
035-os BibID:(WoS)000427631700003 (Scopus)85040654509 (PubMed)29344775
Első szerző:Almássy János (élettanász, biológus, angol-magyar szakfordító)
Cím:New saliva secretion model based on the expression of Na+-K+ pump and K+ channels in the apical membrane of parotid acinar cells / Almássy János, Siguenza Elias, Skaliczki Marianna, Matesz Klara, Sneyd James, Yule David I., Nánási Péter P.
Dátum:2018
ISSN:0031-6768
Megjegyzések:The plasma membrane of parotid acinar cells is functionally divided into apical and basolateral regions. According to the current model, fluid secretion is driven by transepithelial ion gradient, which facilitates water movement by osmosis into the acinar lumen from the interstitium. The osmotic gradient is created by the apical Cl? efflux and the subsequent paracellular Na+ transport. In this model, the Na+-K+ pump is located exclusively in the basolateral membrane and has essential role in salivary secretion, since the driving force for Cl? transport via basolateral Na+?K+?2Cl? cotransport is generated by the Na+-K+ pump. In addition, the continuous electrochemical gradient for Cl? flow during acinar cell stimulation is maintained by the basolateral K+ efflux. However, using a combination of single-cell electrophysiology and Ca2+-imaging, we demonstrate that photolysis of Ca2+ close to the apical membrane of parotid acinar cells triggered significant K+ current, indicating that a substantial amount of K+ is secreted into the lumen during stimulation. Nevertheless, the K+ content of the primary saliva is relatively low, suggesting that K+ might be reabsorbed through the apical membrane. Therefore, we investigated the localization of Na+-K+ pumps in acinar cells. We show that the pumps appear evenly distributed throughout the whole plasma membrane, including the apical pole of the cell. Based on these results, a new mathematical model of salivary fluid secretion is presented, where the pump reabsorbs K+ from and secretes Na+ to the lumen, which can partially supplement the paracellular Na+ pathway.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Parotid acinar cell
Saliva production
Fluid secretion model
Na+-K+ pump
BK channel
maxiK
Gardos channel
Megjelenés:Pflugers Archiv-European Journal Of Physiology. - 470 : 4 (2018), p. 613-621. -
További szerzők:Siguenza, Elias Skaliczki Marianna Matesz Klára (1949-) (anatómus, neurobiológus) Sneyd, James Yule, David I. Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:GINOP-2.3.2-15-2016-00040
GINOP
EFOP-3.6.2-16-2017-00006
EFOP
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2.

001-es BibID:BIBFORM036694
Első szerző:Hegyi Bence (élettanász)
Cím:Tetrodotoxin blocks L-type Ca2+ channels in canine ventricular cardiomyocytes / Bence Hegyi, László Bárándi, István Komáromi, Ferenc Papp, Balázs Horváth, János Magyar, Tamás Bányász, Zoltán Krasznai, Norbert Szentandrássy, Péter P. Nánási
Dátum:2012
ISSN:0031-6768
Megjegyzések:Tetrodotoxin (TTX) is believed to be the mostselective inhibitor of voltage-gated fast Na+ channels inexcitable tissues, including nerve, skeletal muscle, andheart, although TTX sensitivity of the latter is lower thanthe former by at least three orders of magnitude. In thepresent study, the TTX sensitivity of L-type Ca2+ current(ICa) was studied in isolated canine ventricular cells usingconventional voltage clamp and action potential voltageclamp techniques. TTX was found to block ICa in a reversiblemanner without altering inactivation kinetics of ICa.Fitting results to the Hill equation, an IC50 value of55?2 ?M was obtained with a Hill coefficient of unity(1.0?s0.04). The current was fully abolished by 1 ?Mnisoldipine, indicating that it was really ICa. Under actionpotential voltage clamp conditions, the TTX-sensitivecurrent displayed the typical fingerprint of ICa, whichwas absent in the presence of nisoldipine. Stick-and-ballmodels for Cav1.2 and Nav1.5 channel proteins wereconstructed to explain the differences observed betweenaction of TTX on cardiac ICa and INa. This is the firstreport demonstrating TTX to interact with L-type calciumcurrent in the heart.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Calcium channels
Dog heart
Sodium channels
Tetrodotoxin
Voltage clamp
Megjelenés:Pflügers Archiv. - 464 : 2 (2012), p. 167-174. -
További szerzők:Bárándi László (1984-) (élettanász) Komáromi István (1957-) (vegyész, molekuláris biológus, biokémikus) Papp Ferenc (1979-) (biofizikus) Horváth Balázs (1981-) (élettanász) Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Krasznai Zoltán (1950-) (biofizikus) Szentandrássy Norbert (1976-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:K100151
OTKA
PD101171
OTKA
K101196
OTKA
CNK-77855
Egyéb
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3.

001-es BibID:BIBFORM020123
Első szerző:Horváth Balázs (élettanász)
Cím:Contribution of I-Ks to ventricular repolarization in canine myocytes / Balázs Horváth, János Magyar, Norbert Szentandrássy, Péter Birinyi, Péter P. Nánási, Tamás Bányász
Dátum:2006
ISSN:0031-6768
Megjegyzések:The role of the slow delayed rectifier K+ current (I-Ks) in cardiac repolarization seems to be largely influenced by the experimental conditions including the species and tissue studied. The aim of this study was to determine the contribution of I-Ks, to repolarization in canine ventricular myocytes by measuring the frequency dependent action potential lengthening effect of 10 mu M chromanol 293B using sharp microelectrodes. Pretreatment with isoproterenol (2 nM), E-4031 (1 mu M), and injection of inward current pulses were applied to modify action potential configuration. Chromanol alone caused moderate but statistically significant lengthening of action potentials at cycle lengths longer than 500 ms. The lengthening effect of chromanol, which was strongly enhanced in the presence of either isoproterenol or E-4031, was proportional to the amplitude of plateau, whereas poor correlation was found with action potential duration. Similar results were obtained when action potential configuration was modified by injection of depolarizing current pulses. Computer simulations revealed that activation of I-Ks is a sharp function of the plateau amplitude within the physiological range, while elongation of repolarization may enhance I-Ks only when it is excessive. It was concluded that the effect of I-Ks on ventricular repolarization critically depends on the level of action potential plateau; however, other factors, like action potential duration, cycle length, or suppression of other K+ currents can also influence its contribution.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 452 : 6 (2006), p. 698-706. -
További szerzők:Magyar János (1961-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Birinyi Péter (1981-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Bányász Tamás (1960-) (élettanász)
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4.

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

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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6.

001-es BibID:BIBFORM030495
035-os BibID:WOS:A1989AB05200009
Első szerző:Nánási Péter Pál (élettanász)
Cím:Paradox response of frog muscle membrane to changes in external potassium / P. P. Nánási, M. Dankó
Dátum:1989
ISSN:0031-6768
Megjegyzések:Applying conventional microelectrode technique the anomalous behaviour of membrane potential in response to changes in [K+]o was demonstrated in normal and cevadine-treated muscles bathed in Cl- -free medium. Partial repolarization of the cevadine-depolarized membrane and reappearance of the slow membrane potential oscillation (SMPO) were induced by elevating [K+]o from 2.5 mM to 10-20 mM. Both effects were reversed by return to 2.5 mM [K+]o. The K-induced repolarization was markedly reduced by 20 mM Cs+, but not by 0.1 mM ouabain, 1 mM 4-aminopyridine, or 1 mM diethyl-pyrocarbonate. The elevation of [K+]o failed to repolarize muscle fibers that had been depolarized only to a small extent. No K-induced repolarization has been observed in Cl- -containing fluid. In cevadine-free experiments the omission of potassium from the extracellular space in Cl- -free solution hyperpolarized some of the fibers, while depolarized others. Strong electrical stimuli applied in zero K-zero Cl solution turned all the fibers into depolarized state; on returning to 2.5 mM [K+]o complete repolarization was achieved in most of the fibers. It has been concluded that the paradox response of the muscle membrane to changes in [K+]o can be attributed to the K-dependent conductance changes of the inward rectifier K channel providing an explanation for the plateau-formation of SMPO and for the existence of two stable levels of membrane potential of the skeletal muscle bathed in Cl- -free medium.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Pflügers Archiv. - 414 : 2 (1989), p. 157-161. -
További szerzők:Dankó Miklós
Internet cím:DOI
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7.

001-es BibID:BIBFORM014373
Első szerző:Szabó Gergely (élettanász)
Cím:Asymmetrical distribution of ion channels in canine and human left-ventricular wall : epicardium versus midmyocardium / Gergely Szabó, Norbert Szentandrássy, Tamás Bíró, Balázs I. Tóth, Gabriella Czifra, János Magyar, Tamás Bányász, András Varró, László Kovács, Péter P. Nánási
Dátum:2005
ISSN:0031-6768
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Pflügers Archiv. - 450 : 5 (2005), p. 307-316. -
További szerzők:Szentandrássy Norbert (1976-) (élettanász) Bíró Tamás (1968-) (élettanász) Tóth István Balázs (1978-) (élettanász) Czifra Gabriella (1975-) (élettanász) Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Kovács László (1939-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
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8.

001-es BibID:BIBFORM057403
Első szerző:Szentandrássy Norbert (élettanász)
Cím:Contribution of ion currents to beat-to-beat variability of action potential duration in canine ventricular myocytes / Norbert Szentandrássy, Kornél Kistamás, Bence Hegyi, Balázs Horváth, Ferenc Ruzsnavszky, Krisztina Váczi, János Magyar, Tamás Bányász, András Varró, Péter P. Nánási
Dátum:2015
ISSN:0031-6768
Megjegyzések:Although beat-to-beat variability (short-term variability, SV) of action potential duration (APD) is considered as a predictor of imminent cardiac arrhythmias, the underlying mechanisms are still not clear. In the present study, therefore, we aimed to determine the role of the major cardiac ion currents, APD, stimulation frequency, and changes in the intracellular Ca2+ concentration ([Ca2+]i) on the magnitude of SV. Action potentials were recorded from isolated canine ventricular cardiomyocytes using conventional microelectrode techniques. SV was an exponential function of APD, when APD was modified by current injections. Drug effects were characterized as relative SV changes by comparing the drug-induced changes in SV to those in APD according to the exponential function obtained with current pulses. Relative SV was increased by dofetilide, HMR 1556, nisoldipine, and veratridine, while it was reduced by BAY K8644, tetrodotoxin, lidocaine, and isoproterenol. Relative SV was also increased by increasing the stimulation frequency and [Ca2+]i. In summary, relative SV is decreased by ion currents involved in the negative feedback regulation of APD (I Ca, I Ks, and I Kr), while it is increased by I Na and I to. We conclude that drug-induced effects on SV should be evaluated in relation with the concomitant changes in APD. Since relative SV was decreased by ion currents playing critical role in the negative feedback regulation of APD, blockade of these currents, or the beta-adrenergic pathway, may carry also some additional proarrhythmic risk in addition to their well-known antiarrhythmic action.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Short-term variability
Action potential duration
Ion currents
Canine myocytes
Action potential configuration
Doktori iskola
Megjelenés:Pflügers Archiv. - 467 : 7 (2015), p. 1431-1443. -
További szerzők:Kistamás Kornél (1986-) (biológus) Hegyi Bence (1987-) (élettanász) Horváth Balázs (1981-) (élettanász) Ruzsnavszky Ferenc (1984-) (élettanász) Váczi Krisztina (1987-) (élettanász) Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:K10015
OTKA
K109736
OTKA
K101196
OTKA
PD101171
OTKA
NK104331
OTKA
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Élettan Kutatócsoport
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
Molekuláris Orvostudomány Doktori Iskola
TÁMOP-4.2.4.A/2-11/1- 2012-0001
TÁMOP
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