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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.
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


001-es BibID:BIBFORM020122
Első szerző:Magyar János (élettanász)
Cím:L-364,373 fails to activate the slow delayed rectifier K+ current in canine ventricular cardiomyocytes / János Magyar, Balázs Horváth, Tamás Bányász, Norbert Szentandrássy, Péter Birinyi, András Varró, Zsolt Szakonyi, Ferenc Fülöp, Péter P. Nánási
Megjegyzések:Activators of the slow delayed rectifier K+ current (I-Ks) are promising tools to suppress ventricular arrhythmias originating from prolongation of action potentials. A recently synthesized compound, L-364,373, was shown to activate I-Ks in ventricular cells isolated from guinea pigs and rabbits. Due to the interspecies differences known to exist in the properties of the delayed rectifier K+ currents, the effect of L-364,373 on I-Ks was studied and compared with that of another I-Ks activator mefenamic acid in canine ventricular myocytes. Mefenamic acid (100 mu M) significantly increased the amplitude of the fully activated I-Ks current, as well as the I-Ks current tails, by shifting the voltage dependence of its activation towards negative voltages and increased the time constant for deactivation. In contrast, L-364,373, up to concentrations of 3 mu M, failed to augment I-Ks at any membrane potential studied, but slightly increased the time constant of deactivation. It is concluded that human studies are required to evaluate the therapeutically beneficial effects of I-Ks activators. Rodent cardiac tissues are not suitable for this purpose.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Naunyn-Schmiedebergs Archives of Pharmacology. - 373 : 1 (2006), p. 85-89. -
További szerzők:Horváth Balázs (1981-) (élettanász) Bányász Tamás (1960-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Birinyi Péter (1981-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Szakonyi Zsolt Fülöp Ferenc Nánási Péter Pál (1956-) (élettanász)
Internet cím:DOI
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