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1.

001-es BibID:BIBFORM032964
035-os BibID:PMID:8720691
Első szerző:Cseresnyés Z.
Cím:Three different gating models for inactivation of the Ito in ventricular myocytes of rats and mice / Z. Cseresnyés, Z. Rusznák, A. Bozsányi, J. Magyar, G. Szücs, L. Kovács
Dátum:1995
ISSN:0231-5882
Megjegyzések:Kinetic models to describe the time course of the Ca(2+)-independent outward potassium current (Ito) in cardiac ventricular cells were constructed. The Ito traces were recorded from isolated myocytes of rats and mice using the whole-cell configuration of the patch-clamp technique. An iterative method was developed to eliminate the capacitive transient overlapping the early part of the Ito. The isolated Ito curves were then fitted by Hodgkin-Huxley type functions and different inactivation gating mechanisms were identified in various groups of the animals. In some Wistar rats a single inactivation route was found. Another group of Wistar rats and diabetic BB/Mol rats showed two independent inactivation pathways both of which resulted in a completely closed channel. In lean specimen of C-57 mice and in streptozotocin-treated Wistar rats the two inactivation gates gave closed channels only when both parallel inactivating transitions have been completed. In this case a possible interaction between the gating particles has been revealed.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:General Physiology And Biophysics 14 : 4 (1995), p. 259-276. -
További szerzők:Rusznák Zoltán (1965-) (élettanász) Bozsányi A. Magyar János (1961-) (élettanász) Szűcs Géza (1948-) (élettanász) Kovács László (1939-) (élettanász)
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2.

001-es BibID:BIBFORM032962
035-os BibID:PMID:8586253 WOS:A1995TB98900002
Első szerző:Magyar János (élettanász)
Cím:Effects of insulin on potassium currents of rat ventricular myocytes in streptozotocin diabetes / J. Magyar, Z. Cseresnyés, Z. Rusznák, I. Sipos, G. Szücs, L. Kovács
Dátum:1995
ISSN:0231-5882
Megjegyzések:Membrane currents of ventricular cardiomyocytes isolated from control, diabetic and insulin-treated diabetic Wistar rats have been measured using the whole cell configuration of the patch-clamp technique. Insulin restored the density of the 4-aminopyridine-sensitive early transient component of the calcium-independent outward potassium currents which decreased in diabetes. The inactivation rate of the transients increased in diabetes and was normalised by insulin. The late 4-aminopyridine-insensitive component of the outward currents showed the same diabetes- and insulin-related changes. This current could reflect the activation of the delayed rectifier channels although pharmacological identification of this component could not be achieved.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:General Physiology And Biophysics 14 : 3 (1995), p. 191-201. -
További szerzők:Cseresnyés Z. Rusznák Zoltán (1965-) (élettanász) Sipos István Szűcs Géza (1948-) (élettanász) Kovács László (1939-) (élettanász)
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3.

001-es BibID:BIBFORM030258
035-os BibID:WOS:000181565400020
Első szerző:Magyar János (élettanász)
Cím:Differential effects of fluoxetine enantiomers in mammalian neural and cardiac tissues / János Magyar, Zoltán Rusznák, Csaba Harasztosi, Ágnes Körtvély, Pál Pacher, Tamás Bányász, Csaba Pankucsi, László Kovács, Géza Szűcs, Péter P. Nánási, Valéria Kecskeméti
Dátum:2003
ISSN:1107-3756
Megjegyzések:Racemic fluoxetine is a widely used SSRI antidepressant compound having also anticonvulsant effect. In addition, it was shown that it blocked several types of voltage gated ion channels including neural and cardiac calcium channels. In the present study the effects of enantiomers of fluoxetine (R(-)-fluoxetine and S(+)-fluoxetine) were compared on neuronal and cardiac voltage-gated Ca2+ channels using the whole cell configuration of patch clamp techniques, and the anticonvulsant action of these enantiomers was also evaluated in a mouse epilepsy model. In isolated pyramidal neurons of the dorsal cochlear nucleus of the rat the effect of fluoxetine (S(+), R(-) and racemic) was studied on the Ca2+ channels by measuring peak Ba2+ current during ramp depolarizations. All forms of fluoxetine reduced the Ba2+ current of the pyramidal cells in a concentration-dependent manner, with a K, value of 22.3 +/- 3.6 muM for racemic fluoxetine. This value of K, was higher by one order of magnitude than found in cardiac myocytes with fluoxetine enantiomers (2.4 +/- 0.1 and 2.8 +/- 0.2 muM). Difference between the effects of the two enantiomers on neuronal Ba2+, current was observed only at 5 muM concentration: R(-)-fluoxetine inhibited 28 +/- 3% of the peak current, while S(+)-fluoxetine reduced the current by 18 +/- 2% (n=13, P<0.05). In voltage clamped canine ventricular cardiomyocytes both enantiomers of fluoxetine caused a reversible concentration-dependent block of the peak Ca2+ current measured at 0 mV. Significant differences between the two enantiomers in this blocking effect was observed at low concentrations only: S(+)-fluoxetine caused a higher degree of block than R(-)-fluoxetine (56.3 +/- 2.2% versus 49.1 +/- 2.2% and 95.5 +/- 0.9% versus 84.5 +/- 3.1% block with 3 and 10 &mu;M S(+) and R(-)-fluoxetine, respectively, P<0.05, n=5). Studied in current clamp mode, micromolar concentrations of fluoxetine shortened action potential duration of isolated ventricular cells, while higher concentrations also suppressed maximum velocity of depolarization and action potential amplitude. This shortening effect was significantly greater in the case of S(+) than R(-)-fluoxetine at 1 and 3 muM concentrations, whereas no differences in their effects on depolarization were observed. In pentylenetetrazole-induced mouse epilepsy model fluoxetine pretreatment significantly increased the 60 min survival rate, survival duration and seizure latency. These effects were more pronounced with the R(-) than the S(+) enantiomer. The results indicate that fluoxetine exerts much stronger suppressive effect on cardiac than neuronal calcium channels. At micromolar concentrations (between 1 and 10 muM) R(-)-fluoxetine is more effective than the S(+) enantiomer on neuronal, while less effective on cardiac calcium channels. The stronger anticonvulsant effect of the R(-) enantiomer may, at least partially, be explained by these differences. Used as an antidepressant or anticonvulsant drug, less severe cardiac side-effects are anticipated with the R(-) enantiomer.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:International Journal of Molecular Medicine. - 11 : 4 (2003), p. 535-542. -
További szerzők:Rusznák Zoltán (1965-) (élettanász) Harasztosi Csaba Körtvély Ágnes Pacher Pál Bányász Tamás (1960-) (élettanász) Pankucsi Csaba (farmakológus) Kovács László (1939-) (élettanász) Szűcs Géza (1948-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Kecskeméti Valéria
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4.

001-es BibID:BIBFORM024934
Első szerző:Magyar János (élettanász)
Cím:Action potentials and potassium currents in rat ventricular muscle during experimental diabetes / Magyar J., Rusznák Z., Szentesi P., Szűcs G., Kovács L.
Dátum:1992
ISSN:0022-2828
Megjegyzések:Time course of the surface electrical activity was studied in left ventricular trabeculae of Wistar rats made diabetic using streptozotocin. The action potentials were recorded in Tyrode's solution at 32 degrees C, their duration considerably increased in diabetes. By the 8th week, the prolongation was 64% at 25% of repolarization; 112% at 50% and 118% at 75%. Insulin treatment reduced the prolongation of the action potentials although a complete restoration was not achieved. 0.1 mM La3+ moderately shortened the electrical activity both in control and in diabetic trabeculae. Three mM 4-aminopyridine made the time course of control action potentials very similar to the diabetic ones while the action potentials from the diabetic animals were prolonged further to a smaller extent. Whole-cell clamp experiments in isolated ventricular myocytes (20-23 degrees C) showed a considerable decrease and a somewhat accelerated inactivation of the transient outward current (Ito) in diabetes. The steady-state inactivation and the rate of recovery from inactivation of Ito did not change. No alterations in the magnitude and voltage dependence of inward rectifier (IK1) were found around the resting membrane potential. The diabetes-related suppression of Ito explains the decreased repolarization rate of action potentials.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Molecular And Cellular Cardiology. - 24 : 8 (1992), p. 841-853. -
További szerzők:Rusznák Zoltán (1965-) (élettanász) Szentesi Péter (1967-) (élettanász) Szűcs Géza (1948-) (élettanász) Kovács László (1939-) (élettanász)
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5.

001-es BibID:BIBFORM032943
035-os BibID:PMID:9076505
Első szerző:Rusznák Zoltán (élettanász)
Cím:Characteristics of the ventricular transient outward potassium current in genetic rodent models of diabetes / Z. Rusznák, Z. Cseresnyés, I. Sipos, J. Magyar, L. Kovács, G. Szücs
Dátum:1996
ISSN:0231-5882
Megjegyzések:The whole-cell configuration of the patch-clamp technique was employed to measure the transient outward potassium current in enzymatically isolated ventricular cells of spontaneously diabetic rats (BB/Wor) and mice (ob/ob). Healthy littermates (non-diabetic BB rats and lean mice) were used as controls. There was no significant difference between the non-diabetic and diabetic BB rats (Type I diabetes, IDDM) in the amplitude of either the current measured in the absence or the one found in the presence of 4-aminopyridine. The voltage dependence of the activation and steady-state inactivation was also similar in both populations, as no significant difference was observed in the rate of recovery from inactivation of Ito. The amplitudes of the total and 4-aminopyridine sensitive currents of lean and obese mice (Type II diabetes, NIDDM) were also similar. The voltage dependences of the activation and of the steady-state inactivation did not differ significantly, either. Our results might indicate certain limitations of the applicability of experiments carried out on genetically diabetic rats if the results are compared to those derived from the healthy littermates as controls.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:General Physiology And Biophysics 15 : 3 (1996), p. 225-238. -
További szerzők:Cseresnyés Z. Sipos István Magyar János (1961-) (élettanász) Kovács László (1939-) (élettanász) Szűcs Géza (1948-) (élettanász)
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6.

001-es BibID:BIBFORM040573
Első szerző:Szigeti Gyula (élettanász, elektrofiziológus)
Cím:Calcium-activated transient membrane currents are carried mainly by chloride ions in isolated atrial, ventricular and Purkinje cells of rabbit heart / Szigeti Gyula, Rusznák Zoltán, Kovács László, Papp Zoltán
Dátum:1998
ISSN:0958-0670
Megjegyzések:Under physiological conditions, calcium-dependent ([Ca2+]i-dependent) Cl- currents (ICl(Ca)) have been suggested to participate in the repolarizing processes. In this paper, the possible contribution of ICl(Ca) to transient inward currents and, hence to arrhythmias, has been studied in myocytes from the working myocardium and from the conductive system. Single atrial, ventricular and Purkinje cells, isolated enzymatically from rabbit heart, have been studied under whole-cell voltage-clamp and were internally perfused with the fluorescent Ca2+ indicator, fura-2 (100 microM). Ca2+ release from the sarcoplasmic reticulum was either induced by external application of caffeine or occurred spontaneously in Ca(2+)-overloaded cells. Membrane currents accompanying Ca2+ transients showed linear current-voltage characteristics between -60 and +80 mV as evidenced from fast voltage ramps. When intra- and extracellular Cl- concentrations were kept symmetrical in the absence of the Na(+)-Ca2+ exchange mechanism, transient currents had a reversal potential close to 0 mV. Reduction of external Cl- concentration shifted this reversal potential towards the new Cl- equilibrium potential. Neither the time course of the transient currents nor the shift in their reversal potentials was significantly affected by the presence of Na+. Approximately 90% of this current was blocked by the application of the Cl- channel blocker, anthracene-9-carboxylic acid (0.5 mM) at +80 mV. It is concluded, that [Ca2+]i-activated transient membrane currents in atrial, ventricular and Purkinje cells of rabbit heart are mainly due to the activation of a [Ca2+]i-dependent Cl- current.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Experimental Physiology. - 83 : 2 (1998), p. 137-153. -
További szerzők:Rusznák Zoltán (1965-) (élettanász) Kovács László (1939-) (élettanász) Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:ETT T-06424/93
Egyéb
T 016957
OTKA
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