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1.

001-es BibID:BIBFORM030249
035-os BibID:WOS:000187895800005
Első szerző:Bányász Tamás (élettanász)
Cím:Profile of I(Ks) during the action potential questions the therapeutic value of I(Ks) blockade / Tamás Bányász, Roland Koncz, László Fülöp, Norbert Szentandrássy, János Magyar, Péter P. Nánási
Dátum:2004
ISSN:0929-8673
Megjegyzések:The goal of this paper is two fold. First, we attempt to review the reports available on the role Of I-Ks in myocardial repolarization. Based on theoretical considerations and experimental results, it seems reasonable to assume that I-Ks blockade will lengthen the action potential. However, results obtained with I-Ks blockers, like chromanol 293B or L-735,821, are conflicting, since from slight lengthening to marked prolongation of action potentials were equally obtained. Although these contradictory results were explained by interspecies or regional differences, the role Of I-Ks in repolarization is a matter of growing dispute. In the second part of this study, we simulated the performance Of I-Ks during cardiac action potentials. We compared the profile of the predicted current in three mathematical models in order to determine the relative role of the current in repolarization. We studied the effect of the cycle length, action potential duration and height of the plateau on the profile Of I-Ks in epicardiac, endocardiac and midmyocardiac ventricular action potentials. The results indicate that the height of the plateau is the most important parameter to control activation Of I-Ks in cardiac tissues, and accordingly, the interspecies and regional differences observed in the efficacy Of I-Ks blockers are likely due to the known differences in action potential morphology. We conclude also that I-Ks blockade may have unpredictable effects on the length of the action potential in a diseased heart, questioning the possible therapeutic value of drugs blocking I-Ks.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Current Medicinal Chemistry. - 11 : 1 (2004), p. 45-60. -
További szerzők:Koncz Roland Fülöp László (1976-) (kardiológus) Szentandrássy Norbert (1976-) (élettanász) Magyar János (1961-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM020231
035-os BibID: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.
Dátum:2011
ISSN:0929-8673
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
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

3.

001-es BibID:BIBFORM024502
Első szerző:Bányász Tamás (élettanász)
Cím:Mechanism of reverse rate-dependent action of cardioactive agents / Tamás Bányász, László Bárándi, Gábor Harmati, László Virág, Norbert Szentandrássy, Ildikó Márton, Antonio Zaza, András Varró, Péter P. Nánási
Dátum:2011
Megjegyzések:Class 3 antiarrhythmic agents exhibit reverse rate-dependent lengthening of the action potential duration (APD), i.e. changes in APD are greater at longer than at shorter cycle lengths. In spite of the several theories developed to explain this reverse rate-dependency, its mechanism has been clarified only recently. The aim of the present study is to elucidate the mechanisms responsible for reverse rate-dependency in mammalian ventricular myocardium. Action potentials were recorded using conventional sharp microelectrodes from human, canine, rabbit, guinea pig, and rat ventricular myocardium in a rate-dependent manner. Rate-dependent drug-effects of various origin were studied using agents known to lengthen or shorten action potentials allowing thus to determine the drug-induced changes in APD as a function of the cycle length. Both drug-induced lengthening and shortening of action potentials displayed reverse rate-dependency in human, canine, and guinea pig preparations, but not in rabbit and rat myocardium. Similar results were obtained when repolarization was modified by injection of inward or outward current pulses in isolated canine cardiomyocytes. In contrast to reverse rate-dependence, drug-induced changes in APD well correlated with baseline APD values (i.e. that measured before the superfusion of drug or injection of current) in all of the preparations studied. Since the net membrane current (I(net)), determined from the action potential waveform at the middle of the plateau, was inversely proportional to APD, and consequently to cycle length, it is concluded that that reverse rate-dependency may simply reflect the inverse relationship linking I(net) to APD. In summary, reverse rate-dependency is an intrinsic property of drug action in the hearts of species showing positive APD - cycle length relationship, including humans. This implies that development of a pure K(+) channel blocking agent without reverse rate-dependent effects is not likely to be successful.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
antiarrhythmiás szerek
APD
Molekuláris Medicina
egyetemen (Magyarországon) készült közlemény
Megjelenés:Current medicinal chemistry. - 18 : 24 (2011), p. 3597-3606. -
További szerzők:Bárándi László (1984-) (élettanász) Harmati Gábor (1983-) (élettanász) Virág László (élettanász Szeged) Szentandrássy Norbert (1976-) (élettanász) Márton Ildikó (1954-) (fogszakorvos) Zaza, Antonio Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
A feszültségfüggő K-csatornák szerepe excitábilis sejtekben
Internet cím:Szerző által megadott URL
Intézményi repozitóriumban (DEA) tárolt változat
DOI
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4.

001-es BibID:BIBFORM020232
035-os BibID:WOS:000294414700010
Első szerző:Magyar János (élettanász)
Cím:Long term regulation of cardiac L-type calcium channel by small G proteins / Magyar J., Jenes A., Kistamas K., Ruzsnavszky F., Nanasi P. P., Satin J., Szentandrassy N., Banyasz T.
Dátum:2011
ISSN:0929-8673
Megjegyzések:Calcium ions are crucial elements of excitation-contraction coupling in cardiac myocytes. The intracellular Ca(2+) concentration changes continously during the cardiac cycle, but the Ca(2+) entering to the cell serves as an intracellular second messenger, as well. The Ca(2+) as a second messenger influences the activity of many intracellular signalling pathways and regulates gene expression. In cardiac myocytes the major pathway for Ca(2+) entry into cells is L-type calcium channel (LTCC). The precise control of LTCC function is essential for maintaining the calcium homeostasis of cardiac myocytes. Dysregulation of LTCC may result in different diseases like cardiac hypertrophy, arrhytmias, heart failure. The physiological and pathological structural changes in the heart are induced in part by small G proteins. These proteins are involved in wide spectrum of cell biological functions including protein transport, regulation of cell proliferation, migration, apoptosis, and cytoskeletal rearrangement. Understanding the crosstalk between small G proteins and LTCC may help to understand the pathomechanism of different cardiac diseases and to develop a new generation of genetically-encoded Ca(2+) channel inhibitors.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekuláris Medicina
Megjelenés:Current Medicinal Chemistry. - 18 : 24 (2011), p. 3714-3719. -
További szerzők:Jenes Ágnes (1980-) (élettanász) Kistamás Kornél (1986-) (biológus) Ruzsnavszky Ferenc (1984-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Satin, Jonathan Szentandrássy Norbert (1976-) (élettanász) Bányász Tamás (1960-) (élettanász)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
A feszültségfüggő K-csatornák szerepe excitábilis sejtekben
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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5.

001-es BibID:BIBFORM017197
Első szerző:Szentandrássy Norbert (élettanász)
Cím:Powerful technique to test selectivity of agents acting on cardiac ion channels : the action potential voltage-clamp / Norbert Szentandrássy, Dénes Nagy, Ferenc Ruzsnavszky, Gábor Harmati, Tamás Bányász, János Magyar, A. József Szentmiklósi, Péter P. Nánási
Dátum:2011
ISSN:0929-8673
Megjegyzések:Action potential voltage-clamp (APVC) is a technique to visualize the profile of various currents during the cardiacaction potential. This review summarizes potential applications and limitations of APVC, the properties of the mostimportant ion currents in nodal, atrial, and ventricular cardiomyocytes. Accordingly, the profiles ("fingerprints") of themajor ion currents in canine ventricular myocytes, i.e. in cells of a species having action potential morphology and setof underlying ion currents very similar to those found in the human heart, are discussed in details. The degree ofselectivity of various compounds, which is known to be a critical property of drugs used in APVC experiments, isoverviewed. Thus the specificity of agents known to block sodium (tetrodotoxin, saxitoxin), potassium (chromanol293B, HMR 1556, E-4031, dofetilide, sotalol, 4-aminopyridine, BaCl2), calcium (nifedipine, nisolpidine, nicardipine,diltiazem, verapamil, gallopamil), and chloride (anthracene-9-carboxylic acid, DIDS) channels, the inhibitor of thesodium-calcium exchanger (SEA0400), and the activator of sodium current (veratridine) are accordingly discussed.Based on a theory explaining how calcium current inhibitors block calcium channels, the structural comparison of thestudied substances usually confirmed the results of the literature. Using these predictions, a hypothetical super-selectivecalcium channel inhibitor structure was designed. APVC is a valuable tool not only for studying the selectivity of theknown ion channel blockers, but is also suitable for safety studies to exclude cardiac ion channel actions of any agentunder development.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
action potential
action potential voltage-clamp
Molekuláris Medicina
calcium channel
chemical structure
ion current
ion channel blocker
Molekuláris Medicina
selective calcium channel blocker
Megjelenés:Current Medicinal Chemistry. - 18 : 24 (2011), p. 3737-3756. -
További szerzők:Nagy Dénes (1984-) (vegyész) Ruzsnavszky Ferenc (1984-) (élettanász) Harmati Gábor (1983-) (élettanász) Bányász Tamás (1960-) (élettanász) Magyar János (1961-) (élettanász) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:K 73160
OTKA
CNK 77855
OTKA
K 68457
OTKA
TáMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
A feszültségfüggő K-csatornák szerepe excitábilis sejtekben
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Szerző által megadott URL
Borító:
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