Összesen 4 találat.


001-es BibID:BIBFORM020231
035-os BibID:(Scopus)79551587546 (WoS)000294414700009
Első szerző:Bányász Tamás (élettanász)
Cím:Cardiac calmodulin kinase : a potential target for drug design / Banyasz T., Szentandrassy N., Toth A., Nanasi P. P., Magyar J., Chen-Izu Y.
Megjegyzések:Therapeutic strategy for cardiac arrhythmias has undergone a remarkable change during the last decades. Currently implantable cardioverter defibrillator therapy is considered to be the most effective therapeutic method to treat malignant arrhythmias. Some even argue that there is no room for antiarrhythmic drug therapy in the age of implantable cardioverter defibrillators. However, in clinical practice, antiarrhythmic drug therapies are frequently needed, because implantable cardioverter defibrillators are not effective in certain types of arrhythmias (i.e. premature ventricular beats or atrial fibrillation). Furthermore, given the staggering cost of device therapy, it is economically imperative to develop alternative effective treatments. Cardiac ion channels are the target of a number of current treatment strategies, but therapies based on ion channel blockers only resulted in moderate success. Furthermore, these drugs are associated with an increased risk of proarrhythmia, systemic toxicity, and increased defibrillation threshold. In many cases, certain ion channel blockers were found to increase mortality. Other drug classes such as beta-blockers, angiotensin-converting enzyme inhibitors, aldosterone antagonists, and statins appear to have proven efficacy for reducing cardiac mortality. These facts forced researchers to shift the focus of their research to molecular targets that act upstream of ion channels. One of these potential targets is calcium/calmodulin-dependent kinase II (CaMKII). Several lines of evidence converge to suggest that CaMKII inhibition may provide an effective treatment strategy for heart diseases. (1) Recent studies have elucidated that CaMKII plays a key role in modulating cardiac function and regulating hypertrophy development. (2) CaMKII activity has been found elevated in the failing hearts from human patients and animal models. (3) Inhibition of CaMKII activity has been shown to mitigate hypertrophy, prevent functional remodeling and reduce arrhythmogenic activity. In this review, we will discuss the structural and functional properties of CaMKII, the modes of its activation and the functional consequences of CaMKII activity on ion channels.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Current Medicinal Chemistry. - 18 : 24 (2011), p. 3707-3713. -
További szerzők:Szentandrássy Norbert (1976-) (élettanász) Tóth András (farmakológus) Nánási Péter Pál (1956-) (élettanász) Magyar János (1961-) (élettanász) Chen-Izu, Ye
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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)
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001-es BibID:BIBFORM030240
Első szerző:Nagy, Zsolt A.
Cím:Selective inhibition of sodium-calcium exchanger by SEA-0400 decreases early and delayed after depolarization in canine heart / Zsolt A. Nagy, László Virág, András Tóth, Péter Biliczki, Károly Acsai, Tamás Bányász, Péter Nánási, Julius Gy. Papp, András Varro
Megjegyzések:The sodium-calcium exchanger (NCX) was considered to play an important role in arrhythmogenesis under certain conditions such as heart failure or calcium overload. In the present study, the effect of SEA-0400, a selective inhibitor of the NCX, was investigated on early and delayed afterdepolarizations in canine ventricular papillary muscles and Purkinje fibres by applying conventional microelectrode techniques at 37degreesC. The amplitude of both early and delayed afterdepolarizations was markedly decreased by 1 mum SEA-0400 from 26.6 +/- 2.5 to 14.8 +/- 1.8 mV (n = 9, P < 0.05) and from 12.5 &PLUSMN; 1.7 to 5.9 &PLUSMN; 1.4 mV (n = 3, P < 0.05), respectively. In enzymatically isolated canine ventricular myocytes, SEA-0400 did not change significantly the L-type calcium current and the intracellular calcium transient, studied using the whole-cell configuration of the patch-clamp technique and Fura-2 ratiometric fluorometry. It is concluded that, through the reduction of calcium overload, specific inhibition of the NCX current by SEA-0400 may abolish triggered arrhythmias.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:British Journal of Pharmacology. - 143 : 7 (2004), p. 827-831. -
További szerzők:Virág László (élettanász Szeged) Tóth András (farmakológus) Biliczki Péter Acsai Károly Bányász Tamás (1960-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus)
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001-es BibID:BIBFORM065571
Első szerző:Nánási Péter Pál (élettanász)
Cím:Power of the action potential voltage clamp technique / Péter P. Nánási, Norbert Szentandrássy, András Tóth, Tamás Bányász
Tárgyszavak:Orvostudományok Elméleti orvostudományok könyvfejezet
Megjelenés:Advances in Cardiomyocyte Research / Szerk. Nánási Péter P. - p. 93-119. -
További szerzők:Szentandrássy Norbert (1976-) (élettanász) Tóth András (farmakológus) Bányász Tamás (1960-) (élettanász)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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