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001-es BibID:	BIBFORM030253
Első szerző:	Bányász Tamás (élettanász)
Cím:	Different effects of endothelin-1 on calcium and potassium currents in canine ventricular cells / Tamás Bányász, János Magyar, Ágnes Körtvély, Gyula Szigeti, Péter Szigligeti, Zoltán Papp, Attila Mohácsi, László Kovács, Péter P. Nánási
Dátum:	2001
ISSN:	0028-1298
Megjegyzések:	Effects of endothelin-l (ET-1) on the L-type calcium current (I-Ca) and delayed rectifier potassium current (I-K) were studied in isolated canine ventricular cardiomyocytes using the whole-cell configuration of the patch-clamp technique. ET-1 (8 nM) was applied in three experimental arrangements: untreated cells, in the presence of 50 nM isoproterenol, and in the presence of 250 muM 8-bromo-cAMP. In untreated cells, ET-1 significantly decreased the peak amplitude of I-Ca by 32.3 +/-4.8% at +5 mV (P<0.05) without changing activation or inactivation characteristics of I-Ca. ET-1 had no effect on the amplitude of I-K, I-to (transient outward current) or I-K1 (inward rectifier K current) in untreated cells; however, the time course of recovery from inactivation of I-to was significantly increased by ET-1 (from 26.5<plus/minus>6 ms to 59.5 +/- 1.8 ms, P<0.05). Amplitude and time course of intracellular calcium transients, recorded in voltage-clamped cells previously loaded with the fluorescent calcium indicator dye Fura-2, were not affected by ET-1. ET-1 had no effect on force of contraction in canine ventricular trabeculae. Isoproterenol increased the amplitude of I-Ca to 263<plus/minus> 29% of control. ET-1 reduced I-Ca also in isoproterenol-treated cells by 17.8 +/-2% (P<0.05); this inhibition was significantly less than obtained in untreated cells. I-K was increased by isoproterenol to 213<plus/minus>18% of control. This effect of isoproterenol on I-K was reduced by 31.8 +/-4.8% if the cells were pretreated with ET-1. Similarly, in isoproterenol-treated cells ET-1 decreased I-K by 16.2 +/-1.5% (P<0.05). Maximal activation of protein kinase A (PKA) was achieved by application of 8-bromo-cAMP in the pipette solution. In the presence of 8-bromo-cAMP ET-l failed to alter I-CA or I-K It was concluded that differences in effects of ET-1 on I-CA and I-K may be related to differences in cAMP sensitivity of the currents.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Naunyn-Schmiedebergs Archives of Pharmacology. - 363 : 4 (2001), p. 383-390. -
További szerzők:	Magyar János (1961-) (élettanász) Körtvély Ágnes Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Szigligeti Péter Papp Zoltán (1965-) (kardiológus, élettanász) Mohácsi Attila (1960-) (orvos) Kovács László (1939-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
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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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