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1.

001-es BibID:BIBFORM067778
Első szerző:Acsai Károly
Cím:Role of the dysfunctional ryanodine receptor - Na+ -Ca2+ exchanger axis in progression of cardiovascular diseases : what we can learn from pharmacological studies? / Acsai K., Ördög B., Varró A., Nánási P. P.
Dátum:2016
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal of Pharmacology 779 (2016), p. 91-101. -
További szerzők:Ördög Balázs Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
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2.

001-es BibID:BIBFORM001042
Első szerző:Acsai Károly
Cím:Effect of partial blockade of the Na+/Ca2+ - exchanger on Ca2+ handling in isolated rat ventricular myocytes / Károly Acsai, Attila Kun, Attila S. Farkas, Ferenc Fülöp, Norbert Nagy, Marianna Balázs, Norbert Szentandrássy, Péter P. Nánási, Julius Gy. Papp, András Varró, András Tóth
Dátum:2007
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal of Pharmacology. - 576 : 1-3 (2007), p. 1-6. -
További szerzők:Kun Attila Farkas S. Attila Fülöp Ferenc Nagy Norbert (1977-) (kísérletes farmakológus) Balázs Marianna Szentandrássy Norbert (1976-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Tóth András (farmakológus)
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3.

001-es BibID:BIBFORM049179
035-os BibID:PMID:23588116 WOS:000319508800002
Első szerző:Kistamás Kornél (biológus)
Cím:Effects of pioglitazone on cardiac ion currents and action potential morphology in canine ventricular myocytes / Kornél Kistamás, Norbert Szentandrássy, Bence Hegyi, Ferenc Ruzsnavszky, Krisztina Váczi, László Bárándi, Balázs Horváth, Andrea Szebeni, János Magyar, Tamás Bányász, Valéria Kecskeméti, Péter P. Nánási
Dátum:2013
ISSN:0014-2999
Megjegyzések:Despite its widespread therapeutical use there is little information on the cellular cardiac effects of the antidiabetic drug pioglitazone in larger mammals. In the present study, therefore, the concentration-dependent effects of pioglitazone on ion currents and action potential configuration were studied in isolated canine ventricular myocytes using standard microelectrode, conventional whole cell patch clamp, and action potential voltage clamp techniques. Pioglitazone decreased the maximum velocity of depolarization and the amplitude of phase-1 repolarization at concentrations ?3 ?M. Action potentials were shortened by pioglitazone at concentrations ?10 ?M, which effect was accompanied with significant reduction of beat-to-beat variability of action potential duration. Several transmembrane ion currents, including the transient outward K+ current (Ito), the L-type Ca2+ current (ICa), the rapid and slow components of the delayed rectifier K+ current (IKr and IKs, respectively), and the inward rectifier K+ current (IK1) were inhibited by pioglitazone under conventional voltage clamp conditions. Ito was blocked significantly at concentrations ?3 ?M, ICa, IKr, IKs at concentrations ?10 ?M, while IK1 at concentrations ?30 ?M. Suppression of Ito, ICa, IKr, and IK1 has been confirmed also under action potential voltage clamp conditions. ATP-sensitive K+ current, when activated by lemakalim, was effectively blocked by pioglitazone. Accordingly, action potentials were prolonged by 10 ?M pioglitazone when the drug was applied in the presence of lemakalim. All these effects developed rapidly and were readily reversible upon washout. In conclusion, pioglitazone seems to be a harmless agent at usual therapeutic concentrations.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Antidiabetic agents
Pioglitazone
Dog cardiomyocytes
Action potentials
Ion currents
Megjelenés:European Journal of Pharmacology. - 710 : 1-3 (2013), p. 10-19. -
További szerzők:Szentandrássy Norbert (1976-) (élettanász) Hegyi Bence (1987-) (élettanász) Ruzsnavszky Ferenc (1984-) (élettanász) Váczi Krisztina (1987-) (élettanász) Bárándi László (1984-) (élettanász) Horváth Balázs (1981-) (élettanász) Szebeni Andrea Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Kecskeméti Valéria Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:K100151
OTKA
NK104331
OTKA
K101196
OTKA
PD101171
OTKA
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Élettan Kutatócsoport
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4.

001-es BibID:BIBFORM030347
035-os BibID:WOS:A1993LV61600003 PMID:8243533
Első szerző:Lathrop, David A.
Cím:Ionic basis for OPC-8212-induced increase in action potential duration in isolated rabbit, guinea pig and human ventricular myocytes / David A. Lathrop, Péter P. Nanasi, Arnold Schwartz, András Varro
Dátum:1993
ISSN:0014-2999
Megjegyzések:Changes in transmembrane ionic currents induced by OPC-8212 (3,4-dihydro-6-[4-(3,4-dimethoxybenzoyl)-l-piperazinyl]-2(1H)-quinoline) , a recently introduced positive inotropic agent which lengthens cardiac action potential duration, were examined using whole-cell voltage-clamp techniques in single rabbit, guinea pig and human ventricular myocytes. In rabbit, OPC-8212 (12 mumol/l) significantly increased membrane action potential duration measured at 90% of repolarization by an average of 88 ms (from 462 +/- 25 to 550 +/- 35 ms, n = 4; P < 0.05). In rabbit this increase in duration was not associated with significant changes in either the inward rectifier or transient outward K+ currents. The magnitude of the secondary inward current evoked from a holding potential of -50 mV was significantly increased by 97 +/- 8% (n = 6; P < 0.01) while a demonstrable delayed rectifier outward current could not be identified in the rabbit myocytes examined at room temperature. In guinea pig ventricular myocytes, where the delayed rectifier was large, 12 mumol/l OPC-8212 significantly depressed the current by 58 +/- 10% (n = 6; P < 0.01). The effects of OPC-8212 in human ventricular myocytes obtained from the explanted heart of a single patient having an idiopathic cardiomyopathy most closely resembled those observed in isolated rabbit ventricular myocytes. Thus, in rabbit and a few human ventricular myocytes examined at room temperature, OPC-8212 appeared to lengthen cardiac membrane action potential duration primarily by increasing the amplitude of the secondary inward current believed to primarily represent current through L-type Ca2+ channels. In guinea pig preparations, OPC-8212 also decreased the delayed rectifier outward K+ current which also would account for an increase in action potential duration. OPC-8212 could not be demonstrated to affect Na+ current inactivation in a manner similar to that produced by 1 mg/l veratrine, a recognized Na + channel agonist, which dramatically slowed this process.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:European Journal of Pharmacology. - 240 : 2-3 (1993), p. 127-137. -
További szerzők:Nánási Péter Pál (1956-) (élettanász) Schwartz, Arnold Varró András (1954-) (farmakológus, klinikai farmakológus)
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5.

001-es BibID:BIBFORM030245
035-os BibID:WOS:000220687400004
Első szerző:Magyar János (élettanász)
Cím:Effects of terpenoid phenol derivatives on calcium current in canine and human ventricular cardiomyocytes / János Magyar, Norbert Szentandrassy, Tamás Banyasz, László Fülöp, András Varro, Péter P. Nanasi
Dátum:2004
ISSN:0014-2999
Megjegyzések:Concentration-dependent (10-1000 muM) effects of terpenoid phenol derivatives were studied on L-type Ca2+ current in isolated canine and human ventricular cardiomyocytes using the whole-cell configuration of patch clamp technique. Carvacrol, thymol and eugenol suppressed peak Ca2+ current at +5 mV, having EC50 values and Hill coefficients of 98 +/- 11, 158 +/- 7 and 187 +/- 15 muM and 1.42 +/- 0.05, 2.96 +/- 0.43 and 1.6 +/- 0.1, respectively, in canine myocytes. Zingerone displayed a weak effect (estimated EC50: 2 +/- 0.37 mM, Hill coefficient: 0.73 +/- 0.07), while vanillin and guaiacol failed to substantially modify Ca2+ current up to the concentration of I mM. In addition to tonic block, thymol and carvacrol, but not eugenol, evoked marked rate-dependent block at 2 Hz. Carvacrol and eugenol accelerated inactivation of Ca2+ current and caused leftward shift in the voltage dependence of steady-state inactivation without altering activation kinetics. Carvacrol, but not eugenol, increased the time constant of recovery from inactivation. These effects of carvacrol and eugenol developed rapidly and were largely reversible. In myocytes isolated from undiseased human hearts, the effect of carvacrol was similar to that observed in canine cells. It is concluded that suppression of cardiac Ca2+ currents by phenol derivatives is influenced by the substituent in the benzene ring, and the blocking effect of these drugs may involve interactions with the inactivation machinery of the channel. (C) 2004 Elsevier B.V. All rights reserved.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:European Journal of Pharmacology. - 487 : 1-3 (2004), p. 29-36. -
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)
Internet cím:DOI
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6.

001-es BibID:BIBFORM072702
035-os BibID:(WoS)000418522900035 (Scopus)85032657327 (PubMed)29066415
Első szerző:Oravecz Kinga
Cím:Inotropic effect of NCX inhibition depends on the relative activity of the reverse NCX assessed by a novel inhibitor ORM-10962 on canine ventricular myocytes / Kinga Oravecz, Anita Kormos, Andrea Gruber, Zoltán Márton, Zsófia Kohajda, Leila Mirzaei, Norbert Jost, Jouko Levijoki, Piero Pollesello, Tuula Koskelainen, Leena Otsomaa, András Tóth, Julius Gy. Papp, Péter P. Nánási, Gudrun Antoons, András Varró, Károly Acsai, Norbert Nagy
Dátum:2018
ISSN:0014-2999
Megjegyzések:Na+/Ca2+ exchanger (NCX) is the main Ca2+ transporter in cardiac myocytes. Its inhibition could be expected to exert positive inotropic action by accumulation of cytosolic Ca2+ ([Ca2+]i). However, we have observed only a marginal positive inotropic effect upon selective inhibition of NCX, which was enhanced when forward activity was facilitated. Here we attempted to clarify the underlying mechanism of the limited inotropic action of selective NCX inhibition by a novel inhibitor ORM-10962 on canine ventricular myocytes. 1?M ORM-10962 reduced the Ca2+ content of sarcoplasmic reticulum (SR) when the reverse NCX was favoured, while SR Ca2+ content was increased by ORM-10962 under conditions favouring the forward activity, like elevation of [Ca2+]i. L-type Ca2+ current (ICa) was not affected by 1?M ORM-10962 in the absence of SR Ca2+ release, while ICa was suppressed by ORM-10962 during normal Ca2+ cycling. The apparent degree of forward NCX inhibition was dependent on the elevation of [Ca2+]i, suggesting that an increased driving force of forward NCX can also limit the accumulation of [Ca2+i]. We concluded that in healthy myocardium the possible positive inotropic potential of NCX inhibition is considerably weaker than it was expected earlier by theoretical assumptions. The underlying mechanism may involve the autoregulation of Ca2+ handling and/or the preserved inducibility of forward NCX by high [Ca2+]i. This limitation of selective NCX inhibition seen in undiseased myocardium requires further studies in failing heart, which may allow correct evaluation of the potential therapeutic value of selective NCX inhibitors in the treatment of heart failure.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:European Journal of Pharmacology. - 818 (2018), p. 278-286. -
További szerzők:Kormos Anita Gruber Andrea Márton Zoltán Kohajda Zsófia Mirzaei, Leila Jost Norbert Levijoki, Jouko Pollesello, Piero Koskelainen, Tuula Otsomaa, Leena Tóth András Papp Gy. Julius (Szeged) Nánási Péter Pál (1956-) (élettanász) Antoons, Gudrun Varró András (1954-) (farmakológus, klinikai farmakológus) Acsai Károly Nagy Norbert
Pályázati támogatás:NKFIH K-119992
NKFIH
NKFIH K-115397
NKFIH
NKFIH NN109904
NKFIH
NKFIH ANN-113273
NKFIH
NKFIH PD-125402
NKFIH
GINOP-2.3.2-15-2016-00006
GINOP
GINOP-2.3.2-15-2016-00012
GINOP
GINOP-2.3.2-15-2016-040
GINOP
NKFP_07_01-RYT07_AF
Egyéb
UNKP-16-3-IKT/147-1787/8/2016-ÖSZT-95
UNKP
TÁMOP 4.2.4
TÁMOP
EFOP-3.6.2-16-2017-00006.A/2-11-1-2012-0001
EFOP
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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