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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)
Internet cím:	DOI elektronikus változat Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM030336
035-os BibID:	PMID: 15320833
Első szerző:	Mohácsi Attila (orvos)
Cím:	Effects of endothelins on cardiac and vascular cells : new therapeutic target for the future? / Attila Mohácsi, János Magyar, Tamás Bányász, Péter P. Nánási
Dátum:	2004
ISSN:	1570-1611 (Linking)
Megjegyzések:	The predominant isoform of the endothelin peptide family. endothelin-1 (ET-1)exerts various biological effects. These include effects on arterial smoothmuscle cells causing intense vasoconstriction and stimulation of cardiac cells.ET-1 promotes changes in cardiomyocytes that are consistent with electricalremodelling such as changes in ionic current density and inhomogeneousprolongation of action potential duration resulting in increased dispersion. Asfor the underlying mechanisms, ET-1 was shown to suppress several cAMP-dependentionic currents, such as ICa, IK and ICl in various mammalian cardiac preparationsincluding human myocytes; however, the degree of suppression of these currents isdifferent and highly dependent on experimental conditions. The proposedarrhythmogenic effects of ET-1 may also involve enhancement of Ca2+ release fromintracellular stores, generation of IP3, and acidosis due to stimulation of theNa+/H+ exchange. Furthermore, ET-1 acts as the natural counterpart toendothelium-derived nitric oxide, which exerts vasodilator, antithrombotic andantiproliferative effects, and inhibits leukocyte adhesion to the vascular wall.Effects of ET-1 are mediated through interaction with two major types of cellsurface receptors. ETA receptors have been associated with electricalremodelling, vasoconstriction and cell growth, while ETB receptors are involvedin the clearance of ET-1, inhibition of endothelial apoptosis, release of NO andprostacyclins, and inhibition of the expression of ET-1 converting enzyme. Thederangement of endothelial function in various cardiovascular diseases, such ascardiomyopathies, hypertension or arteriosclerosis, is a crucial element of thepathomechanism, thus ET receptors are considered as important therapeutictargets. Indeed, ET receptor antagonists may be able to preserve or restoreendothelial integrity and may have antiarrhythmic properties; therefore, they arepromising tools in cardiovascular medicine.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban 0 (Endothelin-1) 0 (Endothelins) 0 (Protein Isoforms) 0 (Receptors, Endothelin) 7440-70-2 (Calcium) Animals Calcium/*metabolism Electric Stimulation Endothelin-1/adverse effects/metabolism/physiology Endothelins/antagonists & inhibitors/biosynthesis/physiology Humans Muscle, Smooth, Vascular/drug effects/metabolism/physiology Myocardial Contraction/drug effects/physiology Myocytes, Cardiac/drug effects/metabolism Protein Isoforms Receptors, Endothelin/antagonists & inhibitors Signal Transduction/drug effects Vasoconstriction/drug effects/physiology Ventricular Fibrillation/drug therapy egyetemen (Magyarországon) készült közlemény
Megjelenés:	Current vascular pharmacology. - 2 : 1 (2004), p. 53-63. -
További szerzők:	Magyar János (1961-) (élettanász) Bányász Tamás (1960-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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