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1.

001-es BibID:BIBFORM004076
Első szerző:Farkas S. Attila
Cím:Na(+)/Ca(2+) exchanger inhibition exerts a positive inotropic effect in the rat heart, but fails to influence the contractility of the rabbit heart / Farkas A. S., Acsai K., Nagy N., Tóth A., Fülöp F., Seprényi G., Birinyi P., Nánási P. P., Forster T., Csanády M., Papp J. G., Varró A., Farkas A.
Dátum:2008
Megjegyzések:The Na(+)/Ca(2+) exchanger (NCX) may play a key role in myocardial contractility. The operation of the NCX is affected by the action potential (AP) configuration and the intracellular Na(+) concentration. This study examined the effect of selective NCX inhibition by 0.1, 0.3 and 1.0 microM SEA0400 on the myocardial contractility in the setting of different AP configurations and different intracellular Na(+) concentrations in rabbit and rat hearts. EXPERIMENTAL APPROACH: The concentration-dependent effects of SEA0400 on I(Na/Ca) were studied in rat and rabbit ventricular cardiomyocytes using a patch clamp technique. Starling curves were constructed for isolated, Langendorff-perfused rat and rabbit hearts. The cardiac sarcolemmal NCX protein densities of both species were compared by immunohistochemistry. KEY RESULTS: SEA0400 inhibited I(Na/Ca) with similar efficacy in the two species; there was no difference between the inhibitions of the forward or reverse mode of the NCX in either species. SEA0400 increased the systolic and the developed pressure in the rat heart in a concentration-dependent manner, for example, 1.0 microM SEA0400 increased the maximum systolic pressures by 12% relative to the control, whereas it failed to alter the contractility in the rabbit heart. No interspecies difference was found in the cardiac sarcolemmal NCX protein densities. CONCLUSIONS AND IMPLICATIONS: NCX inhibition exerted a positive inotropic effect in the rat heart, but it did not influence the contractility of the rabbit heart. This implies that the AP configuration and the intracellular Na(+) concentration may play an important role in the contractility response to NCX inhibition.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:British Journal of Pharmacology. - 154 : 1 (2008), p. 93-104. -
További szerzők:Acsai Károly Nagy N. (Szeged) Tóth A. Fülöp Ferenc (Szeged) Seprényi G. Birinyi Péter (1981-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Forster Tamás Csanády Miklós (Szeged) Papp J. G. Varró András (1954-) (farmakológus, klinikai farmakológus) Farkas A. (Szeged)
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2.

001-es BibID:BIBFORM013054
Első szerző:Harmati Gábor (élettanász)
Cím:Effects of β-adrenoceptor stimulation on delayed rectifier K(+) currents in canine ventricular cardiomyocytes / Harmati G., Bányász T., Bárándi L., Szentandrássy N., Horváth B., Szabó G., Szentmiklósi J., Szénási G., Nánási P., Magyar J.
Dátum:2011
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
isoproterenol
beta adrenerg
canine
cardiomyocyte
ionic current
Megjelenés:British Journal of Pharmacology. - 162 : 4 (2011), p. 890-896. -
További szerzők:Bányász Tamás (1960-) (élettanász) Bárándi László (1984-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Horváth Balázs (1981-) (élettanász) Szabó G. (orvos) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Szénási Gábor Nánási Péter Pál (1956-) (élettanász) Magyar János (1961-) (élettanász)
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3.

001-es BibID:BIBFORM030281
Első szerző:Knilans, Timothy K.
Cím:Rate and concentration-dependent effects of UK-68,798, a potent new class III antiarrhythmic, on canine Purkinje fibre action potential duration and Vmax / Timothy K. Knilans, David A. Lathrop, Peter P. Nanasi, Arnold Schwartz, Andras Varro
Dátum:1991
ISSN:0007-1188
Megjegyzések:1 The frequency-dependent electrophysiological effects of UK-68,798 in concentrations of 1, 3, 10 and 30 nM were examined in isolated cardiac Purkinje fibres of the dog at both a number of constant rates of stimulation and following abrupt changes in pacing cycle length. 2 In all concentrations evaluated, UK-68,798 lengthened action potential duration in a concentration- and rate-dependent manner (e.g., at a cycle length = 500 ms, control APD90 = 234.0 +/- 3.3 ms, while after 10 nM UK-68,798, APD90 = 315.0 +/- 5.9 ms). 3 The duration of action potentials evoked following abrupt changes in pacing rate were also increased in a concentration-dependent manner at all diastolic intervals tested. 4 The fast and slow time constants for restitution of APD were not altered by UK-68,798. However, the amplitude terms for this relation were increased. 5 In addition, the maximum upstroke velocity (V(max)) was not significantly affected by exposure to UK-68,798 at any concentration or diastolic interval. The kinetics for recovery of V(max) were thus unaffected. 6 These findings are similar to those previously reported for recognized class III antiarrhythmic agents (e.g., bretylium, clofilium, and sotalol); however, UK-68,798 was 1,000 to 10,000 times more potent. 7 The combined potency and selectivity of this agent seem to make it an ideal tool for the investigation of cardiac potassium channels believed responsible for controlling the duration of the action potential. 8 This potent and highly selective compound may prove extremely useful in the control of cardiac arrhythmias.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:British Journal of Pharmacology. - 103 : 2 (1991), p. 1568-1572. -
További szerzők:Lathrop, David A. Nánási Péter Pál (1956-) (élettanász) Schwartz, Arnold Varró András (1954-) (farmakológus, klinikai farmakológus)
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4.

001-es BibID:BIBFORM030261
035-os BibID:WOS:000184795700023
Első szerző:Kovács Anikó
Cím:Beta-adrenoceptor activation plays a role in the reverse rate-dependency of effective refractory period lengthening by dofetilide in the guinea-pig atrium, in vitro / Anikó Kovács, János Magyar, Tamás Bányász, Péter P. Nánási, Gábor Szénási
Dátum:2003
ISSN:0007-1188
Megjegyzések:1 Blockers of the rapid component of the delayed rectifier potassium current (I-Kr) prolong cardiac action potential duration (APD) and effective refractory period (ERP) in a reverse rate-dependent manner. Since activation of beta-adrenoceptors attenuates prolongation of APD evoked by I-Kr blockers, rate-dependent neuronal noradrenaline liberation in the myocardium may contribute to the reverse rate-dependent nature of the effects of I-Kr blockers. In order to test this hypothesis, we studied the effects of dofetilide, a pure I-Kr blocker, on ERP after activation or blockade of beta-adrenoceptors and after catecholamine depletion in guinea-pig left atrial myocardium paced at 3, 2 and 1 Hz, in vitro. 2 Dofetilide (100 nM) lengthened ERP in a reverse rate-dependent manner in the left atrial myocardium of guinea-pigs. Strong activation of beta-adrenoceptors using 10 nM isoproterenol abolished the dofetilide-induced lengthening of ERP at all pacing rates. 3 Blockade of the beta-adrenoceptors with metoprolol (1 muM), atenolol (3 muM) or propranolol (300 nM) increased the dofetilide-evoked prolongation of ERP at 3 and 2 Hz, but not at 1 Hz. As a consequence, metoprolol attenuated while propranolol and atenolol fully eliminated the reverse rate-dependent nature of the dofetilide-induced ERP lengthening. In catecholamine-depleted atrial preparations of the guinea-pig (24 h pretreatment with 5 mg kg(-1) reserpine i.p.), the effect of dofetilide on ERP was not frequency dependent, and propranolol did not alter the effects of dofetilide. 4 In contrast to results obtained in guinea-pig atrial preparations, propranolol failed to change the reverse rate-dependent effect of dofetilide on ERP in the right ventricular papillary muscles of rabbits and guinea-pigs. 5 As an indication of the functional consequences of rate-dependent noradrenaline liberation, propranolol decreased twitch tension at 3 and 2 Hz but not at 1 Hz in the atrial myocardium of control guinea-pigs, whereas no such effect was detected in catecholamine-depleted atrial preparations. Propranolol failed to change contractility of ventricular myocardium in guinea-pigs and rabbits. 6 It is concluded that rate-dependent noradrenaline release and the ensuing beta-adrenoceptor activation contributed to the reverse rate-dependent nature of ERP prolongation caused by I-Kr blockers in isolated guinea-pig atrial myocardium.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:British Journal of Pharmacology. - 139 : 8 (2003), p. 1555-1563. -
További szerzők:Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Szénási Gábor
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5.

001-es BibID:BIBFORM030282
Első szerző:Lathrop, David A.
Cím:In vitro cardiac models of dog Purkinje fibre triggered and spontaneous electrical activity : effects of nicorandil / David A. Lathrop, Péter P. Nánási, András Varró
Dátum:1990
ISSN:0007-1188
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:British Journal of Pharmacology. - 99 : 1 (1990), p. 119-123. -
További szerzők:Nánási Péter Pál (1956-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus)
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6.

001-es BibID:BIBFORM030259
035-os BibID:WOS:000175824200020
Első szerző:Magyar János (élettanász)
Cím:Effects of thymol on calcium and potassium currents in canine and human ventricular cardiomyocytes / János Magyar, Norbert Szentandrássy, Tamás Bányász, László Fülöp, András Varró, Péter P. Nánási
Dátum:2002
ISSN:0007-1188
Megjegyzések:1 Concentration-dependent effects of thymol (1 - 1000 pm) was Studied on action potential configuration and ionic currents in isolated canine ventricular cardiomyocytes using conventional microelectrode and patch clamp techniques. 2 Low concentration of thymol (10 muM) removed the notch of the action potential, whereas high concentrations (100 pm or higher) caused an additional shortening of action potential duration accompanied by progressive depression of plateau and reduction of V-max. 3 In the canine cells L-type Ca current (I-Ca) was decreased by thymol in a concentration-dependent manner (EC50: 158 +/- 7 muM, Hill coeff.: 2.96+/-0.43). In addition. thymol (50 - 250 muM) accelerated the inactivation of I-Ca, increased the time constant of recovery from inactivation, shifted the steady-state inactivation curve of I-Ca leftwards, but voltage dependence of activation remained unaltered. Qualitatively similar results were obtained with thymol in ventricular myocytes isolated from healthy human hearts. 4 Thymol displayed concentration-dependent suppressive effects on potassium currents: the transient outward current, I-10 (EC50: 60.6 +/- 11.4 muM, Hill coeff.: 1.03 +/- 0.11), the rapid component of the delayed rectifier, I-Kr (EC50: 63.4 +/- 6.1 muM, Hill coeff.: 1.29 +/- 0.15), and the slow component of the delayed rectifiers I-Ks (EC50: 202+/-11 muM, Hill coeff.: 0.72+/-0.14), however, K channel kinetics were not much altered by thymol. These effects on Ca and K Currents developed rapidly (within 0.5 min) and were readily reversible. 5 In conclusion, thymol suppressed cardiac ionic channels in a concentration-dependent manner, however, both drug-sensitivities as well as the mechanism of action seems to be different when blocking calcium and potassium channels.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:British Journal of Pharmacology. - 136 : 2 (2002), p. 330-338. -
További szerzők:Szentandrássy Norbert (1976-) (élettanász) Bányász Tamás (1960-) (élettanász) Fülöp László (1976-) (kardiológus) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
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7.

001-es BibID:BIBFORM081896
Első szerző:Nagy Norbert (kísérletes farmakológus)
Cím:Selective Na+/Ca2+ exchanger inhibition prevents Ca2+ overload-induced triggered arrhythmias / Norbert Nagy, Anita Kormos, Zsófia Kohajda, Áron Szebeni, Judit Szepesi, Piero Pollesello, Jouko Levijoki, Károly Acsai, László Virág, Péter P. Nánási, Julius Gy. Papp, András Varró, András Tóth
Dátum:2014
ISSN:0007-1188
Megjegyzések:Background and Purpose Augmented Na+/Ca2+ exchanger (NCX) activity may play a crucial role in cardiac arrhythmogenesis; however, data regarding the anti?arrhythmic efficacy of NCX inhibition are debatable. Feasible explanations could be the unsatisfactory selectivity of NCX inhibitors and/or the dependence of the experimental model on the degree of Ca2+i overload. Hence, we used NCX inhibitors SEA0400 and the more selective ORM10103 to evaluate the efficacy of NCX inhibition against arrhythmogenic Ca2+i rise in conditions when [Ca2+]i was augmented via activation of the late sodium current (INaL) or inhibition of the Na+/K+ pump. Experimental Approach Action potentials (APs) were recorded from canine papillary muscles and Purkinje fibres by microelectrodes. NCX current (INCX) was determined in ventricular cardiomyocytes utilizing the whole?cell patch clamp technique. Ca2+i transients (CaTs) were monitored with a Ca2+?sensitive fluorescent dye, Fluo?4. Key Results Enhanced INaL increased the Ca2+ load and AP duration (APD). SEA0400 and ORM10103 suppressed INCX and prevented/reversed the anemone toxin II (ATX?II)?induced [Ca2+]i rise without influencing APD, CaT or cell shortening, or affecting the ATX?II?induced increased APD. ORM10103 significantly decreased the number of strophanthidin?induced spontaneous diastolic Ca2+ release events; however, SEA0400 failed to restrict the veratridine?induced augmentation in Purkinje?ventricle APD dispersion. Conclusions and Implications Selective NCX inhibition ? presumably by blocking revINCX (reverse mode NCX current) ? is effective against arrhythmogenesis caused by [Na+]i?induced [Ca2+]i elevation, without influencing the AP waveform. Therefore, selective INCX inhibition, by significantly reducing the arrhythmogenic trigger activity caused by the perturbed Ca2+i handling, should be considered as a promising anti?arrhythmic therapeutic strategy.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:British Journal of Pharmacology. - 171 : 24 (2014), p. 5665-5681. -
További szerzők:Kormos Anita Kohajda Zsófia Szebeni Áron Szepesi Judit Pollesello, Piero Levijoki, Jouko Acsai Károly Virág László (élettanász Szeged) Nánási Péter Pál (1956-) (élettanász) Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Tóth András (farmakológus)
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8.

001-es BibID:BIBFORM030240
Első szerző:Nagy, Zsolt A.
Cím:Selective inhibition of sodium-calcium exchanger by SEA-0400 decreases early and delayed after depolarization in canine heart / Zsolt A. Nagy, László Virág, András Tóth, Péter Biliczki, Károly Acsai, Tamás Bányász, Péter Nánási, Julius Gy. Papp, András Varro
Dátum:2004
ISSN:0007-1188
Megjegyzések:The sodium-calcium exchanger (NCX) was considered to play an important role in arrhythmogenesis under certain conditions such as heart failure or calcium overload. In the present study, the effect of SEA-0400, a selective inhibitor of the NCX, was investigated on early and delayed afterdepolarizations in canine ventricular papillary muscles and Purkinje fibres by applying conventional microelectrode techniques at 37degreesC. The amplitude of both early and delayed afterdepolarizations was markedly decreased by 1 mum SEA-0400 from 26.6 +/- 2.5 to 14.8 +/- 1.8 mV (n = 9, P < 0.05) and from 12.5 &PLUSMN; 1.7 to 5.9 &PLUSMN; 1.4 mV (n = 3, P < 0.05), respectively. In enzymatically isolated canine ventricular myocytes, SEA-0400 did not change significantly the L-type calcium current and the intracellular calcium transient, studied using the whole-cell configuration of the patch-clamp technique and Fura-2 ratiometric fluorometry. It is concluded that, through the reduction of calcium overload, specific inhibition of the NCX current by SEA-0400 may abolish triggered arrhythmias.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:British Journal of Pharmacology. - 143 : 7 (2004), p. 827-831. -
További szerzők:Virág László (élettanász Szeged) Tóth András (farmakológus) Biliczki Péter Acsai Károly Bányász Tamás (1960-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus)
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9.

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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10.

001-es BibID:BIBFORM037321
Első szerző:Szentandrássy Norbert (élettanász)
Cím:Effects of rosiglitazone on the configuration of action potentials and ion currents in canine ventricular cells / Szentandrássy N., Harmati G., Bárándi L., Simkó J., Horváth B., Magyar J., Bányász T., Lőrincz I., Szebeni A., Kecskeméti V., Nánási P.P.
Dátum:2011
ISSN:0007-1188
Megjegyzések:BACKGROUND AND PURPOSEIn spite of its widespread clinical application, there is little information on the cellular cardiac effects of the antidiabetic drug rosiglitazone in larger experimental animals. In the present study therefore concentration-dependent effects of rosiglitazone on action potential morphology and the underlying ion currents were studied in dog hearts.EXPERIMENTAL APPROACHStandard microelectrode techniques, conventional whole cell patch clamp and action potential voltage clamp techniques were applied in enzymatically dispersed ventricular cells from dog hearts.KEY RESULTSAt concentrations ?10 mM rosiglitazone decreased the amplitude of phase-1 repolarization, reduced the maximum velocity of depolarization and caused depression of the plateau potential. These effects developed rapidly and were readily reversible upon washout. Rosiglitazone suppressed several transmembrane ion currents, oncentration-dependently, under conventional voltageclamp conditions and altered their kinetic properties. The EC50 value for this inhibition was 25.2 ? 2.7 mM for the transient outward K+ current (Ito), 72.3 ? 9.3 mM for the rapid delayed rectifier K+ current (IKr) and 82.5 ? 9.4 mM for the L-type Ca2+ current (ICa) with Hill coefficients close to unity. The inward rectifier K+ current (IK1) was not affected by rosiglitazone up to concentrations of 100 mM. Suppression of Ito, IKr, and ICa was confirmed also under action potential voltage clamp conditions.CONCLUSIONS AND IMPLICATIONSAlterations in the densities and kinetic properties of ion currents may carry serious pro-arrhythmic risk in case of overdose with rosiglitazone, especially in patients having multiple cardiovascular risk factors, like elderly diabetic patients.
Tárgyszavak:Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban
antidiabetic agents
rosiglitazone
dog cardiomyocytes
action potential
ion currents
Megjelenés:British Journal Of Pharmacology 163 : 3 (2011), p. 499-509. -
További szerzők:Harmati Gábor (1983-) (élettanász) Bárándi László (1984-) (élettanász) Simkó József (1974-) (belgyógyász, kardiológus) Horváth Balázs (1981-) (élettanász) Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Lőrincz István (1950-) (belgyógyász, kardiológus) Szebeni Andrea Kecskeméti Valéria Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
A feszültségfüggő K-csatornák szerepe excitábilis sejtekben
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11.

001-es BibID:BIBFORM037346
Első szerző:Szentandrássy Norbert (élettanász)
Cím:Role of action potential configuration and the contribution of Ca2+ and K+ currents to isoprenaline-induced changes in canine ventricular cells / N. Szentandrássy, V. Farkas, L. Bárándi, B. Hegyi, F. Ruzsnavszky, B. Horváth, T. Bányász, J. Magyar, I. Márton, P. P. Nánási
Dátum:2012
ISSN:0007-1188
Megjegyzések:BACKGROUND AND PURPOSE: Although isoprenaline (ISO) is known to activate several ion currents in mammalian myocardium, little is known about the role of action potential morphology in the ISO-induced changes in ion currents. Therefore, the effects of ISO on action potential configuration, L-type Ca2+ current (ICa), slow delayed rectifier K+ current (IKs) and fast delayed rectifier K+ current (IKr)were studied and compared in a frequency-dependent manner using canine isolated ventricular myocytes from varioustransmural locations.EXPERIMENTAL APPROACHAction potentials were recorded with conventional sharp microelectrodes; ion currents were measured using conventional and action potential voltage clamp techniques.KEY RESULTSIn myocytes displaying a spike-and-dome action potential configuration (epicardial and midmyocardial cells), ISO caused reversible shortening of action potentials accompanied by elevation of the plateau. ISO-induced action potential shortening was absent in endocardial cells and in myocytes pretreated with 4-aminopyridine. Application of the IKr blocker E-4031 failed to modify the ISO effect, while action potentials were lengthened by ISO in the presence of the IKs blocker HMR-1556. Bothaction potential shortening and elevation of the plateau were prevented by pretreatment with the ICa blocker nisoldipine.Action potential voltage clamp experiments revealed a prominent slowly inactivating ICa followed by a rise in IKs, both currents increased with increasing the cycle length.CONCLUSIONS AND IMPLICATIONSThe effect of ISO in canine ventricular cells depends critically on action potential configuration, and the ISO-induced activation of IKs ? but not IKr ? may be responsible for the observed shortening of action potentials
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
heart
action potential
calcium current
potassium current
Megjelenés:British Journal of Pharmacology. - 167 : 3 (2012), p. 599-611. -
További szerzők:Farkas Viktória Bárándi László (1984-) (élettanász) Hegyi Bence (1987-) (élettanász) Ruzsnavszky Ferenc (1984-) (élettanász) Horváth Balázs (1981-) (élettanász) Bányász Tamás (1960-) (élettanász) Magyar János (1961-) (élettanász) Márton Ildikó (1954-) (fogszakorvos) Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
A feszültségfüggő K-csatornák szerepe excitábilis sejtekben
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

12.

001-es BibID:BIBFORM016885
Első szerző:Virág László (élettanász Szeged)
Cím:Analysis of the contribution of Ito to repolarization in canine ventricular myocardium / Virág L., Jost N., Papp R., Koncz I., Kristóf A., Kohajda Z., Harmati G., Carbonell-Pascual B., Ferrero J. M. Jr., Papp J. Gy., Nánási P. P., Varró A.
Dátum:2011
ISSN:0007-1188
Megjegyzések:Contribution of the transient outward potassium current (Ito) to ventricular repolarization is controversial depending on the experimental conditions, the region of myocardium or the species studied. The aim of the present study was, therefore, to characterize Ito and estimate its contribution to repolarization reserve in canine ventricular myocardium. Experimental approach: Ion currents were recorded using conventional whole cell voltage clamp and action potential voltage clamp techniques in isolated canine ventricular cells. Action potentials were recorded from canine ventricular preparations using microelectrodes. Key results: Contribution of Ito to repolarization was studied using 100 ?M chromanol 293B in full IKs blockade by 0.5 ?M HMR 1556. This high concentration of chromanol 293B effectively suppressed Ito without affecting other repolarizing K(+) currents (IK1, IKr, Ip). Action potential clamp experiments revealed a slowly inactivating and a "late" chromanol-sensitive current component flowing during the action potential plateau. Action potentials were significantly lengthened by chromanol 293B in the presence of HMR 1556. This lengthening effect of Ito inhibition showed reverse rate-dependent properties. It was extremely augmented after additional attenuation of repolarization reserve by 0.1 ?M dofetilide resulting in the occurrence of early afterdepolarizations (EADs). The results have been confirmed by computer simulation. Conclusions and Implications: The results indicate that Ito is involved in governing repolarization in canine ventricular myocardium and, it contributes significantly to the repolarization reserve. Therefore, blockade of Ito may enhance proarrhythmic risk.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
transient outward current
action potential duration
repolarization reserve
cardiac ventricular muscle
arrhythmia
Megjelenés:British Journal Of Pharmacology. - 164 : 1 (2011), p. 93-105. -
További szerzők:Jost Norbert Papp R. Koncz István (Szeged) Kristóf A. (Szeged) Kohajda Zsófia Harmati Gábor (1983-) (élettanász) Carbonell-Pascual, B. Ferrero, J. M. Jr Papp Gy. Julius (Szeged) Nánási Péter Pál (1956-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus)
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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