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001-es BibID:	BIBFORM040624
Első szerző:	Papp Zoltán (kardiológus, élettanász)
Cím:	Calcium-dependent modulation of the plateau phase of action potential in isolated ventricular cells of rabbit heart / Papp Z., Peineau N., Szigeti G., Argibay J., Kovács L.
Dátum:	1999
ISSN:	0001-6772
Megjegyzések:	[Ca2+]i-dependent modulation of the action potential has been studied in Fura-2 dialysed ventricular myocytes of the rabbit using the whole-cell current-clamp method. Fifteen consecutive action potentials (AP1-AP15) and [Ca2+]i transients were elicited at a frequency of 0.2 Hz. A single, brief application of caffeine (during AP9) first enhanced and thereafter attenuated the [Ca2+]i transients accompanying AP9 and AP10-AP12, respectively. This approach provided direct comparison between time courses of action potentials: during the initial steady state (e.g. AP8) and when Ca2+ release from the sarcoplasmic reticulum was increased by caffeine (AP9) or decreased by depletion (AP10). The increase in [Ca2+]i facilitated repolarization and decreased action potential duration. However, action potentials at reduced Ca2+ release (AP10) had longer duration than during steady state. The caffeine-induced changes in L-type Ca2+ current (ICa,L), during voltage-clamp conditions partially explained the effects of caffeine on action potentials. When ICa,L was blocked by 500 micromol L-1 Cd2+, enhanced [Ca2+]i transients revealed an extra current component which was outward at +10 mV and inward at the resting membrane potential (most probably the transient inward current). In the presence of Cd2+, however, AP8 and AP10 had identical time courses, suggesting that ICa,L alone was responsible for the lengthening of AP10. Alterations in the transmembrane Na+ gradient resulted in changes of the steady state action potential durations (AP8) consistently with the expected modulation of the Na+-Ca2+ exchange current. However, the contribution of this current to the [Ca2+]i-dependent behaviour of action potential plateau could not be demonstrated.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Acta Physiologica Scandinavica. - 167 : 2 (1999), p. 119-129. -
További szerzők:	Peineau, N. Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Argibay, J. Kovács L.
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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)
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