CCL

Összesen 5 találat.
#/oldal:
Részletezés:
Rendezés:

1.

001-es BibID:BIBFORM004074
Első szerző:Birinyi Péter (élettanász)
Cím:The Na+/Ca2+ exchange blocker SEA0400 fails to enhance cytosolic Ca2+ transient and contractility in canine ventricular cardiomyocytes / Birinyi P., Tóth A., Jóna I., Acsai K., Almássy J., Nagy N., Prorok J., Gherasim I., Papp Z., Hertelendi Z., Szentandrássy N., Bányász T., Fülöp F., Papp J. G., Varró A., Nánási P. P., Magyar J.
Dátum:2008
Megjegyzések:Aims This study was designed to evaluate the effects of the Na+/Ca2+ exchange (NCX) inhibitor SEA0400 on Ca2+ handling in isolated canine ventricular myocytes. Methods and results Intracellular Ca2+ ([Ca2+](i)) transients, induced by either field stimulation or caffeine flush, were monitored using Ca2+ indicator dyes. [Ca2+](i)-dependent modulation of the inhibitory effect of SEA0400 on NCX was characterized by the changes in Ni2+-sensitive current in voltage-clamped myocytes. Sarcoplasmic reticulum (SR) Ca2+ release and uptake were studied in SIR membrane vesicles. Gating properties of single-ryanodine receptors were analysed in lipid bilayers. Ca2+ sensitivity of the contractile machinery was evaluated in chemically skinned myocytes. In myocytes paced at 1 Hz, neither diastolic [Ca2+](i) nor the amplitude of [Ca2+](i) transients was significantly altered by SEA0400 up to the concentration of 1 mu M, which was shown to inhibit the exchange current. The blocking effect of SEA0400 on NCX decreased with increasing [Ca2+](i), and it was more pronounced in reverse than in forward mode operation at every [Ca2+](i) examined. The rate of decay of the caffeine-induced [Ca2+](i) transients was decreased significantly by 1 mu M SEA0400; however, this effect was only a fraction of that observed with 10 mM NiCl2. Neither SR Ca2+ release and uptake nor cell shortening and Ca2+ sensitivity of the contractile proteins were influenced by SEA0400. Conclusion The lack of any major SEA0400-induced shift in Ca2+ transients or contractility of myocytes can well be explained by its limited inhibitory effect on NCX (further attenuated by elevated [Ca2+](i) levels) and a concomitant reduction in Ca2+ influx due to the predominantly reverse mode blockade of NCX and suppression of L-type Ca2+ current.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cardiovascular Research. - 78 : 3 (2008), p. 476-484. -
További szerzők:Tóth András (farmakológus) Jóna István (1948-) (élettanász, fizikus) Acsai Károly Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító) Nagy Norbert (1977-) (kísérletes farmakológus) Prorok János Gherasim, Iuliana Papp Zoltán (1965-) (kardiológus, élettanász) Hertelendi Zita (1978-) (orvos) Szentandrássy Norbert (1976-) (élettanász) Bányász Tamás (1960-) (élettanász) Fülöp Ferenc Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász) Magyar János (1961-) (élettanász)
Internet cím:elektronikus változat
DOI
Borító:

2.

001-es BibID:BIBFORM073611
Első szerző:Hegyi Bence (élettanász)
Cím:Complex electrophysiological remodeling in postinfarction ischemic heart failure / Bence Hegyi, Julie Bossuyt, Leigh G. Griffiths, Rafael Shimkunas, Zana Coulibaly, Zhong Jian, Kristin N. Grimsrud, Claus S. Sondergaard, Kenneth S. Ginsburg, Nipavan Chiamvimonvat, Luiz Belardinelli, András Varró, Julius G. Papp, Piero Pollesello, Jouko Levijoki, Leighton T. Izu, W. Douglas Boyd, Tamás Bányász, Donald M. Bers, Ye Chen-Izu
Dátum:2018
ISSN:0027-8424 1091-6490
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Proceedings Of The National Academy Of Sciences Of The United States Of America 115 : 13 (2018), p. E3036-E3044. -
További szerzők:Bossuyt, Julie Griffiths, Leigh G. Shimkunas, Rafael Coulibaly, Zana Jian, Zhong Grimsrud, Kristin N. Sondergaard, Claus S. Ginsburg, Kenneth S. Chiamvimonvat, Nipavan Belardinelli, Luiz Varró András (1954-) (farmakológus, klinikai farmakológus) Papp Gy. Julius (Szeged) Pollesello, Piero Levijoki, Jouko Izu, Leighton T. Boyd, W. Douglas Bányász Tamás (1960-) (élettanász) Bers, Donald M. Chen-Izu, Ye
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

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

4.

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

5.

001-es BibID:BIBFORM030339
035-os BibID:PMID: 8899061 WOS:A1996VL12100005
Első szerző:Nánási Péter Pál (élettanász)
Cím:Electrical restitution in rat ventricular muscle / P. P. Nanasi, Cs. Pankucsi, T. Banyasz, P. Szigligeti, J. Gy. Papp, A. Varro
Dátum:1996
ISSN:0001-6772
Megjegyzések:The mechanism of electrical restitution was studied in isolated rat ventricular muscle using drugs that inhibit specific ion currents. The effect of transient changes in cytosolic Ca concentration and Na/Ca exchange in relation to the restitution process was also studied in single ventricular cardiomyocytes. Conventional microelectrode techniques were applied to record action potentials having gradually increasing coupling intervals. each evoked following a train of stimuli with a frequency of 1 Hz. ion currents were recorded from enzymatically isolated cells using the whole cell parch clamp technique. Ca transients were monitored in myocytes loaded with the fluorescent dye, indo-1. The electrical restitution process in multicellular rat ventricular preparations at 37 degrees C was described as a sum oi three exponential components: an early positive component. a subsequent fast negative component and a late negative component. having time constants of 21.9 +/- 1.9, 73.1 +/- 6.0 and 1053 +/- 61 ms, respectively (n = 9). Inhibition of the transient outward K current the delayed rectifier K current. or the chloride current did not substantially alter these time constants, The early positive and fast negative components were fully abolished by nifedipine or MnCl2. In the presence of caffeine. the fast negative component was absent. while the time constant of the early positive component increased to 39.5 +/- 5.8 ms (n = 5). In single myocytes loaded with indo-1, the Ca transients decayed with a time constant of 151 +/- 12 ms at room temperature (n = 5). These Ca transients were accompanied by inward current tails. identified as a Na/Ca exchange current. having a decay time constant of 140 +/- 4.5 ms. It is concluded that electrical restitution in rat ventricular muscle is relatively little affected by recovery from voltage-dependent inactivation of ion channels. it is rather governed by transient changes in cytosolic Ca concentration possible via Ca-dependent inactivation of the L-type Ca current and activation of the Na/Ca exchange current.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Acta Physiologica Scandinavica. - 158 : 2 (1996), p. 143-153. -
További szerzők:Pankucsi Csaba (farmakológus) Bányász Tamás (1960-) (élettanász) Szigligeti Péter Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus)
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1 
Corvina könyvtári katalógus v8.2.27 © 2023 Monguz kft. Minden jog fenntartva.