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1.

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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2.

001-es BibID:BIBFORM030263
035-os BibID:WOS:000168774300010
Első szerző:Jednákovits Andrea
Cím:In vivo and in vitro acute cardiovascular effects of bimoclomol / Andrea Jednákovits, Péter Ferdinándy, László Jaszlits, Tamás Bányász, János Magyar, Péter Szigligeti, Ágnes Körtvély, József A. Szentmiklósi, Péter P. Nánási
Dátum:2000
ISSN:0306-3623
Megjegyzések:Effects of bimoclomol, the novel heat shock protein (HSP) coinducer, was studied in various mammalian cardiac and rabbit aortic preparations. Bimoclomol decreased the ST-segment elevation induced by coronary occlusion in anesthetized dogs (56% and 80% reduction with 1 and 5 mg/kg, respectively). In isolated working rat hearts, bimoclomol increased coronary now (CF), decreased the reduction of cardiac output (CO) and left ventricular developed pressure (LVDP) developing after coronary occlusion, and prevented ventricular fibrillation (VF) during reperfusion. In rabbit aortic preparations, precontracted with phenylephrine, bimoclomol induced relaxation (EC50=214 muM). Bimoclomol produced partial relaxation against 20 mM KCl, however, bimoclomol failed to relax preparations precontracted with serotonin, PGF(2) or angiotensin II. All these effects were evident within a few minutes after application of bimoclomol. A rapid bimoclomol-induced compartmental translocation of the already preformed HSPs may explain the protective action of the compound. (C) 2001 Elsevier Science Inc. All rights reserved.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:General Pharmacology-the Vascular System. - 34 : 5 (2000), p. 363-369. -
További szerzők:Ferdinándy Péter Jaszlits László Bányász Tamás (1960-) (élettanász) Magyar János (1961-) (élettanász) Szigligeti Péter Körtvély Ágnes Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Nánási Péter Pál (1956-) (élettanász)
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3.

001-es BibID:BIBFORM030267
Első szerző:Körtvély Ágnes
Cím:Cardiovascular effects of BRX-005 comparison to bimoclomol / Ágnes Körtvély, Gyula Szigeti, Rudolf Gesztelyi, Judit Zsuga, Tamás Bányász, János Magyar, Péter Szigligeti, László Kovács, Andrea Jednákovits, A. József Szentmiklósi, Péter P. Nánási
Dátum:2000
ISSN:0024-3205
Megjegyzések:Concentration-dependent effects of BRX-005, the novel heat shock protein coinducer, cardioprotective and vasoprotective agent, on intracellular calcium transients and contractility were studied in Langendorff-perfused guinea pig hearts loaded with the fluorescent calcium indicator dye Fura-2. BRX-005 increased peak left ventricular pressure, the rate of force development and relaxation significantly in a concentration-dependent manner. The amplitude of [Ca2+](i) transients was left unaltered by the drug, in contrast to BRX-005, bimoclomol increased both contractility and the amplitude of [Ca2+](i) transients, In canine ventricular cardiomyocytes high concentrations of BRX-005 had no effect on depolarization, whereas bimoclomol suppressed action potential upstroke markedly. In guinea pig pulmonary artery preparations precontracted with phenylephrine, BRX-005 induced concentration-dependent relaxation. This effect of BRX-005 was independent of the integrity of endothelium indicating that vasorelaxant effect of the drug develops directly on vascular smooth muscle, (C) 2000 Elsevier Science Inc. All rights reserved.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Life Sciences. - 67 : 14 (2000), p. 1783-1789. -
További szerzők:Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Gesztelyi Rudolf (1969-) (kísérletes farmakológus) Zsuga Judit (1973-) (neurológus, pszichoterapeuta, egészségügyi szakmanager) Bányász Tamás (1960-) (élettanász) Magyar János (1961-) (élettanász) Szigligeti Péter Kovács László (1939-) (élettanász) Jednákovits Andrea Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Nánási Péter Pál (1956-) (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:BIBFORM030265
035-os BibID:WOS:000085470500011
Első szerző:Magyar János (élettanász)
Cím:Electrophysiological effects of bimoclomol in canine ventricular myocytes / János Magyar, Tamás Bányász, Péter Szigligeti, Ágnes Körtvély, Andrea Jednákovits, Péter P. Nánási
Dátum:2000
ISSN:0028-1298
Megjegyzések:Concentration-dependent effects of bimoclomol, a novel heat shack protein (HSP) coinducer, were studied on the parameters of action potential and transmembrane ionic currents in enzymatically dispersed canine ventricular cardiomyocytes using conventional microelectrode and whole cell voltage clamp techniques. Bimoclomol (10-100 mu M) decreased the maximum velocity of depolarization ((V) over dot(max)) and amplitude of action potentials in a concentration-dependent manner. These effects were fully reversible after a 5-min period of washout in drug-free medium. Action potential duration measured at 50% or 90% level of repolarization (APD-50 and APD-90, respectively) was markedly shortened by bimoclomol. Both APD-50 and APD-90 were decreased, but the reduction in APD-50 was more pronounced. The APD-shortening effect of bimoclomol was significantly reduced in the presence of 20 nM charybdotoxin (inhibitor of the Ca-dependent K current) or 0.5 mM anthracene-9-carboxylic acid (inhibitor of the Ca-dependent Cl current) or 1 mu M glibenclamide (inhibitor of the ATP-sensitive K current). In the presence of anthracene-9-carboxylic acid, APD-90 was lengthened by bimoclomol. The APD-shortening effect of bimoclomol was also partially antagonized by chelation of intracellular Ca2+ by application of the cell permeant form of BAPTA, or when using 10 mM EGTA-containing patch pipettes to record action potentials. The (V) over dot(max)-depressant effect of bimoclomol was not affected by charybdotoxin, anthracene-9-carboxylic acid, glibenclamide, or BAPTA load. In voltage clamped cardiomyocytes bimoclomol (100 mu M) had no effect all the amplitude of I-Ca, but decreased significantly the inactivation time constant of I-Ca (from 19.8+/-1.6 ms to 16.8+/-1.2 ms at 0 mV). Bimoclomol also decreased significantly the amplitude of I-K1 (from -20.5+/-1.1 pA/pF to -16.6+/-0.8 pA/pF at -135 mV), causing reduction in slope of the negative branch of the I-V curve. At positive potentials, however, bimoclomol increased outward current. The bimoclomol-induced current, therefore, was studied in the presence of BaCl2, when I-K1 current was blocked. The bimoclomol-induced current had a reversal potential close to -90 mV. Bimoclomol (100 mu M) had no effect on the amplitude or kinetic properties of the transient outward K current (I-to) and the delayed rectifier K current (I-K). It is concluded that bimoclomol exerts both Ca-independent (inhibition of I-Na and I-K1, activation of the ATP-sensitive K current) and Ca-dependent effects (mediated by Ca-activated Cl and probably K currents) in canine ventricular myocytes.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Naunyn-Schmiedebergs Archives of Pharmacology. - 361 : 3 (2000), p. 303-310. -
További szerzők:Bányász Tamás (1960-) (élettanász) Szigligeti Péter Körtvély Ágnes Jednákovits Andrea Nánási Péter Pál (1956-) (élettanász)
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6.

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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7.

001-es BibID:BIBFORM030257
035-os BibID:WOS:000169039300004
Első szerző:Magyar János (élettanász)
Cím:Effects of the antiarrhythmic agent EGIS-7229 (S 21407) on calcium and potassium currents in canine ventricular cardiomyocytes / János Magyar, Tamás Bányász, László Fülöp, Norbert Szentandrássy, Ágnes Körtvély, Anikó Kovács, Gábor Szénási, Péter P. Nánási
Dátum:2001
ISSN:0028-1298
Megjegyzések:Based on earlier pharmacological studies performed using conventional microelectrodes EGIS-7229 (S 21407), the novel antiarrhythmic candidate, was suggested to have a combined mode of action in cardiac tissues isolated from various mammalian species. In order to characterize the electrophysiological effects of the compound, its effects on calcium and potassium currents of isolated canine ventricular cardiomyocytes were studied in the present work using the whole cell configuration of the patch clamp technique. L-type Ca current (I-Ca) was significantly depressed by EGIS-7229 at concentrations of 3 muM or higher with no concomitant changes in the voltage-dependence of activation and time course of inactivation of I-Ca. The drug reversibly suppressed the rapid component of the delayed rectifier K current (I-Kr) in a concentration-dependent manner, having a K-0.5 value of 1.1+/-0.1 muM and a slope factor of close to unity (1.23+/-0.16), indicating that probably one single binding site of high affinity may be involved in binding of EGIS-7229 to the I-Kr channel. In contrast, no changes in the slow component of the delayed rectifier K current (I-Ks,) was observed with the compound up to the concentration of 100 muM, even if the current was fully activated by 8-bromo-cAMP. At a concentration of 10 muM or higher, EGIS-7229 caused also a moderate but significant reduction in the inward rectifier K current (I-K1) and the transient outward K current (I-to) with no change in the voltage-dependence of activation and steady-state inactivation of I-to. Present results indicate that EGIS-7229 can be considered as a selective I-Kr blocker at low (1 muM) concentration; however, its combined (class III + IV) mechanism of action is evident at concentrations of 3 muM or higher. Suppression of I-Ca may explain the lack of development of early afterdepolarizations in the presence of EGIS-7229, predicting a relatively safe clinical application in contrast to pure class III compounds.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Naunyn-Schmiedebergs Archives of Pharmacology. - 363 : 6 (2001), p. 604-611. -
További szerzők:Bányász Tamás (1960-) (élettanász) Fülöp László (1976-) (kardiológus) Szentandrássy Norbert (1976-) (élettanász) Körtvély Ágnes Kovács Anikó Szénási Gábor Nánási Péter Pál (1956-) (élettanász)
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8.

001-es BibID:BIBFORM030264
035-os BibID:WOS:000086138300017
Első szerző:Nánási Péter Pál (élettanász)
Cím:Biphasic effect of bimoclomol on calcium handling in mammalian ventricular myocardium / Péter P. Nánási, Sándor Sárközi, Gyula Szigeti, István Jóna, Csaba Szegedi, Ágnes Szabó, Tamás Bányász, János Magyar, Péter Szigligeti, Ágnes Körtvély, László Csernoch, László Kovács, Andrea Jednákovits
Dátum:2000
ISSN:0007-1188
Megjegyzések:1 Concentration-dependent effects of bimoclomol, the novel heat shock protein coinducer, on intracellular calcium transients and contractility were studied in Langendorff-perfused guinea-pig hearts loaded with the fluorescent calcium indicator dye Fura-2. Bimoclomol had a biphasic effect on contractility: both peak left ventricular pressure and the rate of force development significantly increased at a concentration of 10 nM or higher. The maximal effect was observed between 0.1 and 1 mu M, and the positive inotropic action disappeared by further increasing the concentration of bimoclomol. The drug increased systolic calcium concentration with a similar concentration-dependence. In contrast, diastolic calcium concentration increased monotonically in the presence of bimoclomol. Thus low concentrations of the drug (10-100 nM) increased, whereas high concentrations (10 mu M) decreased the amplitude of intracellular calcium transients. 2 Effects of bimoclomol on action potential configuration was studied in isolated canine ventricular myocytes. Action potential duration was increased at low (10 nM), unaffected at intermediate (0.1-1 mu M) and decreased at high (10-100 mu M) concentrations of the drug. 3 In single canine sarcoplasmic calcium release channels (ryanodine receptor), incorporated into artificial lipid bilayer, bimoclomol significantly increased the open probability of the channel in the concentration range of 1-10 mu M. The increased open probability was associated with increased mean open time. The effect of bimoclomol was again biphasic: the open probability decreased below the control level in the presence of 1 mM bimoclomol. 4 Bimoclomol (10 mu M-1 mM) had no significant effect on the rate of calcium uptake into sarcoplasmic reticulum vesicles of the dog, indicating that in vivo calcium reuptake might not substantially be affected by the drug. 5 In conclusion, the positive inotropic action of bimoclomol is likely due to the activation of the sarcoplasmic reticulum calcium release channel in mammalian ventricular myocardium.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:British Journal of Pharmacology. - 129 : 7 (2000), p. 1405-1412. -
További szerzők:Sárközi Sándor (1966-) (élettanász) Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Jóna István (1948-) (élettanász, fizikus) Szegedi Csaba Szabó Ágnes Bányász Tamás (1960-) (élettanász) Magyar János (1961-) (élettanász) Szigligeti Péter Körtvély Ágnes Csernoch László (1961-) (élettanász) Kovács László (1939-) (élettanász) Jednákovits Andrea
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Borító:

9.

001-es BibID:BIBFORM030269
Első szerző:Szigeti Gyula (élettanász, elektrofiziológus)
Cím:Effects of bimoclomol, the novel heat shock protein coinducer, in dog ventricular myocardium / Gyula Szigeti, Tamás Bányász, János Magyar, Ágnes Körtvély, Péter Szigligeti, László Kovács, Andrea Jednákovits, Péter P. Nánási
Dátum:2000
ISSN:0024-3205
Megjegyzések:The effects of the novel HSP-coinducer bimoclomol was studied on action potentials, ionic currents and [Ca2+](i) transients in isolated canine ventricular myocytes using conventional microelectrode techniques and whole cell voltage clamp combined with fluorescent [Ca2+](i) measurements. Contractility was studied in right ventricular trabeculae, All preparations were paced with a frequency of 0.2 Hz. Bimoclomol (100 mu M) shortened action potential duration measured at 50% repolarization, but lengthened action potentials at the 90% repolarization level, decreased action potential amplitude and maximum depolarization velocity in a reversible manner. In voltage clamped myocytes, the drug activated a steady-state outward current at positive membrane potentials leaving the peak inward current unaffected, [Ca2+](i) transients, measured under voltage clamp control, were increased in amplitude and had accelerated decay kinetics in the presence of the compound, in addition to reduction of diastolic [Ca2+](i). Bimoclomol significantly decreased the force of contraction in right ventricular trabeculae. Comparison of present data to previous results indicate that the cardiac effects of bimoclomol strongly depend on actual experimental conditions. The reduced contractility in spite of the increased amplitude of [Ca2+](i) transients suggests that 100 mu M bimoclomol may decrease calcium sensitivity of the contractile apparatus. (C) 2000 Elsevier Science Inc. All rights reserved.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Life Sciences. - 67 : 1 (2000), p. 73-79. -
További szerzők:Bányász Tamás (1960-) (élettanász) Magyar János (1961-) (élettanász) Körtvély Ágnes Szigligeti Péter Kovács László (1939-) (élettanász) Jednákovits Andrea Nánási Péter Pál (1956-) (élettanász)
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