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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:BIBFORM072791
Első szerző:Barta Tünde
Cím:Endothelin-1-induced hypertrophic alterations and heme oxygenase-1 expression in cardiomyoblasts are counteracted by beta estradiol : in vitro and in vivo studies / Tunde Barta, Agnes Tosaki, David Haines, Gyorgy Balla, Istvan Lekli, Arpad Tosaki
Dátum:2018
ISSN:0028-1298
Megjegyzések:Endothelin-1(ET-1),apotentvasoconstrictornormallyactiveinmaintainingvasculartone,maymediatesignificantpathogeniceffects, contributing to several serious diseases when aberrantly expressed or regulated. The present study evaluates the capacity of ET-1 to affect endothelin-1-associated hypertrophic activity and decreased expression of heme oxygenase-1 by H9c2 rat cardiomyoblasts in vitro, corresponding to in vivo processes underlying cardiovascular diseases (CVDs). Beta estradiol (?-E) is tested for its capacity to altertheeffectsofET-1.H9c2cells,cultured48h,werestimulatedwith100?10,000 nM of ET-1andevaluatedfor changes incell size,cellviability,andexpressionofthecytoprotectiveheatshockproteinhemeoxygenase-1(HO-1),with200nMof?-Eincludedin selectedculturestoevaluateitseffectonET-1-mediatedchanges.Theapplicationof100to10,000nMofET-1resultedinasignificant increase in average cell size and decreases in both cell viability and HO-1 protein content (p<0.05). Moreover, 200 nM of ?-E was observedtosignificantlycounteracttheseeffectsbycardiomyoblastsstimulatedwith1000nMofET-1(p<0.05).Sprague-Dawleyrats treated intravenously with 1000 ng/kg of ET-1 demonstrated reduced HO-1 expression in peripheral blood and left ventricular tissue, whichwascounteractedbyinjectionof200ng/kg?-E?demonstratingapossiblecorrespondencebetweeninvitroandinvivoeffects. Anoutcomeofparticularvalueforclinicaluseof ?-E,inthemanagementofcardiachypertrophy,istheobservedcapacityofthedrug to abate ET-1-mediated suppression of HO-1 expression. It has been previously demonstrated that HO-1 inducers exhibit potent cardioprotective properties, thus offering the promise of combining them with ?-E, allowing lower effective dosage of the drug and concomitantly lower adverse side effects associated with its clinical use. Major findings of this investigation are that pretreatment of cardiomyoblasts with ?-E inhibited their hypertrophic response to ET-1 and counteracts the decrease of cell viability. These effects were associated with a restoration of HO-1 protein expression in both under in vitro and in vivo conditions.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
endothelin
H9c2
Beta-estradiol
Megjelenés:Naunyn-Schmiedebergs Archives Of Pharmacology. - 391 : 4 (2018), p. 371-383. -
További szerzők:Tósaki Ágnes (1992-) (bőrgyógyász) Haines, David Donald (1981-) (gyógyszerész) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Lekli István (1981-) (gyógyszerész) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Pályázati támogatás:OTKA-104017
OTKA
GINOP-2.3.2-15-2016-00043
GINOP
K104017
OTKA
NKFIH-124719
NKFIH
PD-111794
OTKA
TÁMOP-4.2.4. A/2-11-1-2012-0001
TÁMOP
GINOP-2.3.2-15-2016-00043
GINOP
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3.

001-es BibID:BIBFORM024618
Első szerző:Benkő Ilona (orvos, farmakológus)
Cím:Effect of myelopoietic and pleiotropic cytokines on colony formation by blast cells of children with acute lymphoblastic leukemia / Ilona Benkő, Péter Kovács, István Szegedi, Attila Megyeri, Attila Kiss, Erzsébet Balogh, Éva Oláh, János Kappelmayer, Csongor Kiss
Dátum:2001
ISSN:0028-1298
Megjegyzések:The aim of this study was to see whether pleiotropic or myeloid hematopoietic growth factors, which do not stimulate normal lymphoid cells, can induce proliferation of blast cells of the acute lymphoid leukemia (ALL) of childhood. Bone marrow cells of 13 children with untreated ALL (nine common ALL, two myeloid antigen positive ALL and two early T-cell ALL) formed colonies of leukemic blast cells in primary methylcellulose cultures. Spontaneous growth was observed in three of 13 cases, whereas phytohemagglutinin-stimulated leukocyte conditioned medium (PHA-LCM), a conventional source of various natural human cytokines, induced colony formation in ten of 13 cases. A similar rate of responsiveness was seen with recombinant human granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF) and stem cell factor (SCF); a combination of these three cytokines induced colony formation in all cases studied. The effect of these growth factors on colony formation seemed to be dose-dependent in some cases. Of the stimuli studied, GM-CSF induced the smallest number of colonies, whereas the effects of G-CSF, SCF and PHA-LCM were similar in this respect. Combination of cytokines proved to be even more efficient in inducing clonal proliferation of leukemic lymphoblasts. In double combinations, G-CSF and GM-CSF as well as G-CSF and SCF were able to potentiate each other's effects. Triple combination of these cytokines mediated the most potent growth stimulus. Our results demonstrate that myeloid and pleiotropic cytokines are able to stimulate clonal proliferation of pediatric leukemic lymphoblasts. This may present a potential hazard to children with ALL while on adjuvant therapy with hematopoietic growth factors. In vitro colony assays performed prior to or in parallel with the administration of hematopoietic growth factors to ALL patients may help to forecast their possible effects on leukemic cells in vivo.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Naunyn-Schmiedebergs Archives Of Pharmacology 363 : 5 (2001), p. 499-508. -
További szerzők:Kovács Péter (1939-) (farmakológus) Szegedi István (1969-) (hematológus, onkológus, nefrológus) Megyeri Attila (1968-) (orvos) Kiss Attila (1942-) (belgyógyász, haematológus) Balogh Erzsébet (1949-) (biológus, citogenetikus) Oláh Éva (1943-2019) (gyermekgyógyász, klinikai genetikus) Kappelmayer János (1960-) (laboratóriumi szakorvos) Kiss Csongor (1956-) (hematológus, onkológus)
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DOI
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4.

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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5.

001-es BibID:BIBFORM042841
035-os BibID:PMID:23474828
Első szerző:Drimba László (farmakológus)
Cím:The role of acute hyperinsulinemia in the development of cardiac arrhythmias / László Drimba, Róbert Döbrönte, Csaba Hegedüs, Réka Sári, Yin Di, Joseph Németh, Zoltán Szilvássy, Barna Peitl
Dátum:2013
Megjegyzések:Patients with perturbed metabolic control are more prone to develop cardiac rhythm disturbances. The main purpose of the present preclinical study was to investigate the possible role of euglycemic hyperinsulinemia in development of cardiac arrhythmias. Euglycemic hyperinsulinemia was induced in conscious rabbits equipped with a right ventricular pacemaker electrode catheter by hyperinsulinemic euglycemic glucose clamp (HEGC) applying two different rates of insulin infusion (5 and 10 mIU/kg/min) and variable rate of glucose infusion to maintain euglycemia (5.5±0.5 mmol/l). The effect of hyperinsulinemia on cardiac electrophysiological parameters was continuously monitored by means of 12-lead surface ECG recording. Arrhythmia incidence was determined by means of programmed electrical stimulation (PES). The possible role of adrenergic activation was investigated by determination of plasma catecholamine levels and intravenous administration of a beta adrenergic blocking agent, metoprolol. All of the measurements were performed during the steady-state period of HEGC and subsequent to metoprolol administration. Both 5 and 10 mIU/kg/min insulin infusion prolonged significantly QTend, QTc, and Tpeak-Tend intervals. The incidence of ventricular arrhythmias generated by PES was increased significantly by euglycemic hyperinsulinemia and exhibited linear relationship to plasma levels of insulin. No alteration on plasma catecholamine levels could be observed; however, metoprolol treatment restored the prolonged QTend, QTc, and Tpeak-Tend intervals and significantly reduced the hyperinsulinemia-induced increase of arrhythmia incidence. Euglycemic hyperinsulinemia can exert proarrhythmic effect presumably due to the enhancement of transmural dispersion of repolarization. Metoprolol treatment may be of benefit in hyperinsulinemia associated with increased incidence of cardiac arrhythmias.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Naunyn-Schmiedeberg's Archives of Pharmacology. - 386 : 5 (2013), p. 435-444. -
További szerzők:Döbrönte Róbert Hegedűs Csaba (1983-) (Molekuláris biológus, Cera-Med Kft. Debrecen) Sári Réka (farmakológus) Di, Yin Németh József (1954-) (vegyész, analitikus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus)
Pályázati támogatás:GOP-1.2.1-08-2009-0023
Egyéb
NKFP_07-A2-2008-0260
Egyéb
GOP-1.1.2-07/1-2008-0004
Egyéb
TÁMOP-4.2.2.-08/1-2008-0014
TÁMOP
OM-00174/2008
Egyéb
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
GOP-1.1.1-07/1- 2008-0032
Egyéb
OTKA-75965
OTKA
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6.

001-es BibID:BIBFORM013055
Első szerző:Harmati Gábor (élettanász)
Cím:Effects of the PKC inhibitors chelerythrine and bisindolylmaleimide I (GF 109203X) on delayed rectifier K(+) currents / Harmati G., Papp F., Szentandrássy N., Bárándi L., Ruzsnavszky F., Horváth B., Bányász T., Magyar J., Panyi G., Krasznai Z., Nánási P. P.
Dátum:2011
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
isoproterenol
beta adrenerg
canine
cardiomyocyte
ionic current
PKA
PKC
Molekuláris Medicina
Megjelenés:Naunyn-Schmiedeberg's Archives of Pharmacology. - 383 : 2 (2011), p. 141-148. -
További szerzők:Papp Ferenc (1979-) (biofizikus) Szentandrássy Norbert (1976-) (élettanász) Bárándi László (1984-) (élettanász) Ruzsnavszky Ferenc (1984-) (élettanász) Horváth Balázs (1981-) (élettanász) Bányász Tamás (1960-) (élettanász) Magyar János (1961-) (élettanász) Panyi György (1966-) (biofizikus) Krasznai Zoltán (1950-) (biofizikus) Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:K 68457
OTKA
K 75904
OTKA
K 73160
OTKA
CNK 77855
OTKA
MEC-14/2008
EGYÉB
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
A feszültségfüggő K-csatornák szerepe excitábilis sejtekben
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7.

001-es BibID:BIBFORM070843
Első szerző:Horváth Balázs (élettanász)
Cím:Frequency-dependent effects of omecamtiv mecarbil on cell shortening of isolated canine ventricular cardiomyocytes / Horváth B., Szentandrássy N., Veress R., Almássy J., Magyar J., Bányász T., Tóth A., Papp Z., Nánási P. P.
Dátum:2017
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Naunyn-Schmiedeberg's archives of pharmacology. - 390 : 2 (2017), p. 1239-1246. -
További szerzők:Szentandrássy Norbert (1976-) (élettanász) Veress Roland (1992-) (molekuláris biológus) Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Tóth Attila (1971-) (biológus) Papp Zoltán (1965-) (kardiológus, élettanász) Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:K115397
NKFIH
K109736
NKFIH
K101196
NKFIH
PD120794
NKFIH
GINOP-2.3.2-15-2016-00040
GINOP
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8.

001-es BibID:BIBFORM061365
Első szerző:Kovács Diána Klára (Molekuláris biológus)
Cím:Meal-induced insulin sensitization is preserved after acute olanzapine administration in female Sprague-Dawley rats / Diána Kovács, Csaba Hegedűs, Rita Kiss, Réka Sári, József Németh, Zoltán Szilvássy, Barna Peitl
Dátum:2015
ISSN:0028-1298
Megjegyzések:Olanzapine, an atypical antipsychotic, can acutely induce fasting insulin resistance, but we do not know whether it is able to modulate the meal-induced insulin sensitization (MIS). Two main experimental groups (control and olanzapine-treated) were created with two subgroups (fasted and re-fed) within each. After oral vehicle/olanzapine administration, the first meal size and duration and the total amount of consumed food was recorded in conscious rats. Then, under anaesthesia, the carotid artery and jugular vein was prepared and cannulated to obtain samples for blood glucose and hormone determination as well as for insulin/glucose infusion, respectively. Basal insulin sensitivity and MIS was determined by homeostasis model assessment (HOMA) calculation and by rapid insulin sensitivity test, respectively. In fasted animals, olanzapine increased blood glucose and plasma insulin and reduced basal insulin sensitivity, but it failed to modify other hormone levels. Postprandial leptin and glucose-dependent insulinotropic polypeptide (GIP) levels increased, and ghrelin level decreased significantly (p?<?0.05) both in vehicle- and olanzapine-treated groups, but plasma insulin increased only in vehicle-treated animals. Furthermore, decrement in ghrelin level was attenuated in olanzapine-treated animals compared to controls. There was no significant change in the first meal size and duration or in the total amount of food consumed. Olanzapine had no effect on the MIS. We demonstrated that olanzapine can induce insulin resistance without weight gain in healthy rats. Furthermore, the MIS was preserved after acute olanzapine treatment. The blunted postprandial ghrelin and insulin response could contribute to the effect of olanzapine on feeding behaviour. Pharmacological induction of MIS may improve the olanzapine-induced insulin resistance.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Olanzapine
Insulin sensitivity
Satiety
Ghrelin
Gut hormones
Megjelenés:Naunyn-Schmiedebergs Archives Of Pharmacology. - 388 : 5 (2015), p. 525-530. -
További szerzők:Hegedűs Csaba (1983-) (Molekuláris biológus, Cera-Med Kft. Debrecen) Kiss Rita (1974-) (laboratóriumi diagnosztika szakorvos) Sári Réka (farmakológus) Németh József (1954-) (vegyész, analitikus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus)
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9.

001-es BibID:BIBFORM027563
Első szerző:Kovács Péter (belgyógyász, kardiológus, klinikai farmakológus)
Cím:Non-specific caspase inhibition reduces infarct size and improves post-ischaemic recovery in isolated ischaemic/reperfused rat hearts / Peter Kovacs, Istvan Bak, Levente Szendrei, Miklos Vecsernyes, Edit Varga, Ingolf E. Blasig, Arpad Tosaki
Dátum:2001
Megjegyzések:Myocardial ischaemia and reperfusion lead to myocardial cell death due, at least in part, to apoptotic mechanisms. Although cysteinyl aspartate-specific proteinase (caspase) activation is a major event and the most-cited culprit in the development of apoptosis, its potential contribution to ischaemic myocardial cell death is largely unknown. To study the role of caspase activation, isolated rat hearts (n=6 per group) were subjected to 30 min coronary artery occlusion followed by 120 min reperfusion. A non-selective [0.1 or 0.5 microM acetyl-Tyr-Val-Ala-Asp chloromethylketone (YVAD-cmk)] or selective caspase inhibitors [0.07 or 0.2 microM acetyl-Asp-Glu-Val-Asp-cmk (Ac-DEVD-cmk, caspase-3 inhibitor); 0.07 or 0.2 microM benzoxycarbonyl-Leu-Glu-OMe-His-Asp(OMe)-fluoromethylketone (z-LEHD-fmk, caspase-9 inhibitor)] were added to the perfusate at the start of reperfusion. Non-selective caspase inhibition with 0.1 or 0.5 microM YVAD-cmk limited infarct size: (21 +/- 4%, P<0.05; 17 +/- 3%, P<0.05, respectively) compared with the ischaemic/reperfused control (32 +/- 5%). In hearts treated with 0.1 or 0.5 microM caspase II non-selective inhibitor, the fraction of terminal-deoxynucleotidyl-transferase deoxyuridine nick end labelling (TUNEL)-positive myocyte nuclei in the infarcted zone was reduced from the ischaemic/reperfused non-treated control of 11.2 +/- 2.1% to 6.2 +/- 1.6% (P<0.05) and 1.2 +/- 0.2% (P<0.05), respectively. The recovery of post-ischaemic cardiac function (coronary flow, aortic flow and left-ventricular developed pressure) improved significantly with the application of the non-selective caspase inhibitor as well. In hearts perfused with specific caspase inhibitors (caspase-3 and caspase-9) there was no significant reduction in the infarct size, no improvement in post-ischaemic cardiac function and no reduction of apoptotic cell death. We conclude that non-specific inhibition of caspases may be therapeutically beneficial in myocardial ischaemia/reperfusion-induced damage, while selective caspase inhibitors may fail to prevent such reperfusion-induced injury in our model system.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Naunyn-Schmiedeberg's archives of pharmacology 364 : 6 (2001), p. 501-507. -
További szerzők:Bak István (1975-) (vegyész, analitikus, farmakológus) Szendrei Levente Vecsernyés Miklós (1959-) (gyógyszertechnológus, endokrinológus) Varga Edit (gyógyszerész) Blasig, Ingolf E. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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10.

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)
Internet cím:DOI
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11.

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)
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

12.

001-es BibID:BIBFORM030256
035-os BibID:WOS:000178499200009
Első szerző:Magyar János (élettanász)
Cím:Electrophysiological effects of risperidone in mammalian cardiac cells / János Magyar, Tamás Bányász, Zsolt Bagi, Pál Pacher, Norbert Szentandrássy, László Fülöp, Valéria Kecskeméti, Péter P. Nánási
Dátum:2002
ISSN:0028-1298
Megjegyzések:In this study, the effects of risperidone, the widely used antipsychotic drug, on isolated canine ventricular myocytes and guinea-pig papillary muscles were analyzed using conventional microelectrode and whole cell voltage-clamp techniques. Risperidone concentration-dependently lengthened action potential duration in guinea-pig papillary muscles (EC50=0.29 +/- 0.02 muM) and single canine ventricular myocytes (EC50=0.48 +/- 0.14 muM). This effect was reversible, showed reverse rate dependence, and it was most prominent on the terminal portion of repolarization. No significant effect of risperidone on the resting membrane potential, action potential amplitude or maximum rate of depolarization was observed. In voltage-clamped canine ventricular myocytes risperidone caused concentration-dependent block of the rapid component of the delayed rectifier K+ current (1(Kr)), measured as outward current tails at -40 mV with an IC50 of 0.92 +/- 0.26 muM. Suppression of I-Kr was not associated with changes in activation or deactivation kinetics. High concentration of risperidone (10 muM) suppressed also the slow component of the delayed rectifier K+ current (I-Ks) by 9.6 +/- 1.5% at +50 mV. These effects of risperidone developed rapidly and were readily reversible. Risperidone had no significant effect on the amplitude of other K+ currents (I-K1 and I-to). The inhibition of cardiac I-Kr current by risperidone may explain the cardiac side-effects observed occasionally with the drug. Our results suggest that risperidone displays class III antiarrhythmic properties, and as such, may produce QTc prolongation, especially in patients with long QT syndrome. Therefore, in psychotic patients having also cardiac disorders, ECG control may be suggested during risperidone therapy.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Naunyn-Schmiedebergs Archives of Pharmacology. - 366 : 4 (2002), p. 350-356. -
További szerzők:Bányász Tamás (1960-) (élettanász) Bagi Zsolt (1974-) (orvos) Pacher Pál Szentandrássy Norbert (1976-) (élettanász) Fülöp László (1976-) (kardiológus) Kecskeméti Valéria Nánási Péter Pál (1956-) (élettanász)
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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