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001-es BibID:	BIBFORM004111
Első szerző:	Szentandrássy Norbert (élettanász)
Cím:	SEA0400 fails to alter the magnitude of intracellular Ca2+ transients and contractions in Langendorff-perfused guinea pig hearts / Szentandrássy N., Birinyi P., Szigeti Gy., Farkas A., Magyar J., Tóth A., Csernoch L., Varró A., Nánási P.P.
Dátum:	2008
Megjegyzések:	SEA0400 is a recently developed inhibitor of the Na+/Ca2+ exchanger (NCX) shown to suppress both forward and reverse mode operation of NCX. Present experiments were designed to study the effect of partial blockade of NCX on Ca handling and contractility in Langendorff-perfused guinea pig hearts loaded with the fluorescent Ca-sensitive dye fura-2. Left ventricular pressure and intracellular calcium concentration ([Ca2+]i) were synchronously recorded before and after cumulative superfusion with 0.3 and 1 muM SEA0400. SEA0400 caused no significant change in the systolic and diastolic values of left ventricular pressure and [Ca2+]i. Accordingly, pulse pressure and amplitude of the [Ca2+]i transient also remained unchanged in the presence of SEA0400. SEA0400 had no influence either on the time required to reach peak values of pressure and [Ca2+)]i or on half relaxation time. On the other hand, both 0.3 and 1 microM SEA0400 significantly increased the decay time constant of [Ca2+]i transients, obtained by fitting its descending limb between 30% and 90% of relaxation, from 127 +/- 7 to 165 +/- 7 and 177 +/- 14 ms, respectively (P < 0.05, n=6). In contrast to the guinea pig hearts, rat hearts responded to SEA0400 treatment with increased [Ca2+]i transients and contractility. These interspecies differences observed in the effect of SEA0400 can be explained by the known differences in calcium handling between the two species.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Naunyn-Schmiedeberg's Archives of Pharmacology. - 378 : 1 (2008), p. 65-71. -
További szerzők:	Birinyi Péter (1981-) (élettanász) Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Farkas Attila (1961-) (farmakológus) Magyar János (1961-) (élettanász) Tóth András (farmakológus) Csernoch László (1961-) (élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
Internet cím:	elektronikus változat DOI
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001-es BibID:	BIBFORM030276
035-os BibID:	WOS:000074327800003
Első szerző:	Szigligeti Péter
Cím:	Intracellular calcium and electrical restitution in mammalian cardiac cells / P. Szigligeti, T. Banyasz, J. Magyar, Gy. Szigeti, Z. Papp, A. Varro, P. P. Nanasi
Dátum:	1998
ISSN:	0001-6772
Megjegyzések:	The role of calcium current and changes in intracellular calcium concentration ([Ca(2+)](i)) in regulation of action potential duration (APD) during electrical restitution process was studied in mammalian ventricular preparations. Properly timed action potentials were recorded from multicellular preparations and isolated cardiomyocytes using conventional microelectrodes and EGTA-containing patch pipettes, APD increased monotonically in canine and guinea pig ventricular preparations with increasing diastolic interval (DI), while in rabbit papillary muscles the restitution process was biphasic: APD first lengthened, then shortened as the DI increased. When the restitution process was studied in single cardiomyocytes using EGTA-containing patch pipettes, the restitution pattern was similar in the three species studied. Similarly, no difference was observed in the recovery time constant of calcium current (/(Ca-L)) measured under these conditions in voltage clamped myocytes. Loading the myocytes with the [Ca(2+)](i)-chelator BAPTA-AM had adverse effects in rabbit and canine cells. In rabbit myocytes steady-state APD lengthened and the late shortening component of restitution was abolished in BAPTA-loaded cells. In canine myocytes BAPTA-load shortened steady-stare APD markedly, and during restitution, APD decreased with increasing DI. The late shortening component of restitution, observed in untreated rabbit preparations, was greatly reduced after nifedipine treatment, but remained preserved in the presence of 4-aminopyridine or nicorandil. Beat to beat changes in APD, peak /Ca-L and [Ca(2+)](i), measured using the fluorescent dye, Fura-2, were monitored in rabbit ventricular myocytes after a 1-min period of rest. In these cells, the shortening of APD was accompanied by a gradual reduction of the peak /Ca-L and elevation of diastolic [Ca(2+)](i) during the initial eight post-rest action potentials. it is concluded that elevation of [Ca(2+)](i) shortens, while reduction of [Ca(2+)](i) lengthens APD in rabbit, but not in canine ventricular myocytes. These differences may probably be related.io different distributions of [Ca(2+)](i)-dependent ion currents and/or to differences in calcium handling between the two species.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Acta Physiologica Scandinavica. - 163 : 2 (1998), p. 139-147. -
További szerzők:	Bányász Tamás (1960-) (élettanász) Magyar János (1961-) (élettanász) Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Papp Zoltán (1965-) (kardiológus, élettanász) Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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