@article{MTMT:33689741,
	title = {Role of protein kinase A and calcium/calmodulin-dependent protein kinase II in beta-adrenergic regulation of potassium channels in canine ventricular cardiomyocytes},
	url = {https://m2.mtmt.hu/api/publication/33689741},
	author = {Horváth, Balázs and Kiss, Dénes Zsolt and Veress, Roland and Kovács, Zsigmond Máté and Dienes, Csaba Bálint and Szentandrássy, Norbert and Bányász, Tamás and Magyar, János and Nánási, Péter Pál},
	doi = {10.1016/j.yjmcc.2022.08.290},
	journal-iso = {J MOL CELL CARDIOL},
	journal = {JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY},
	volume = {173},
	unique-id = {33689741},
	issn = {0022-2828},
	year = {2022},
	eissn = {1095-8584},
	pages = {S148},
	orcid-numbers = {Horváth, Balázs/0000-0003-2562-8446; Szentandrássy, Norbert/0000-0003-0197-9567}
}

@article{MTMT:33134113,
	title = {Role of protein kinase A and calcium/calmodulin-dependent protein kinase II in beta-adrenergic regulation of potassium channels},
	url = {https://m2.mtmt.hu/api/publication/33134113},
	author = {Horváth, Balázs and Kiss, Dénes Zsolt and Hézső, Tamás and Veress, Roland and Dienes, Csaba Bálint and Kovács, Zsigmond Máté and Szentandrássy, Norbert and Magyar, János and Bányász, Tamás and Nánási, Péter Pál},
	journal-iso = {ACTA PHYSIOL},
	journal = {ACTA PHYSIOLOGICA},
	volume = {236},
	unique-id = {33134113},
	issn = {1748-1708},
	year = {2022},
	eissn = {1748-1716},
	pages = {103-105},
	orcid-numbers = {Horváth, Balázs/0000-0003-2562-8446; Szentandrássy, Norbert/0000-0003-0197-9567}
}

@article{MTMT:32246276,
	title = {The role of action potential restitution versus Ca2+ cycling in the mechanism of alternans in canine ventricular myocardium},
	url = {https://m2.mtmt.hu/api/publication/32246276},
	author = {Nagy, Norbert and Tóth, Noémi and Kohajda, Zsófia and Szlovák, Jozefina and Bitay, Gergő and Veress, Roland and Horváth, Balázs and Papp, Gyula and Varró, András},
	journal-iso = {SCRIPTA MEDICA},
	journal = {SCRIPTA MEDICA},
	volume = {52},
	unique-id = {32246276},
	issn = {1211-3395},
	year = {2021},
	pages = {S72},
	orcid-numbers = {Horváth, Balázs/0000-0003-2562-8446; Varró, András/0000-0003-0745-3603}
}

@article{MTMT:32153454,
	title = {The development of L-type Ca2+ current mediated alternans does not depend on the restitution slope in canine ventricular myocardium},
	url = {https://m2.mtmt.hu/api/publication/32153454},
	author = {Tóth, Noémi and Szlovák, Jozefina and Kohajda, Zsófia and Bitay, Gergő and Veress, Roland and Horváth, Balázs and Papp, Gyula and Varró, András and Nagy, Norbert},
	doi = {10.1038/s41598-021-95299-7},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {11},
	unique-id = {32153454},
	issn = {2045-2322},
	abstract = {Cardiac alternans have crucial importance in the onset of ventricular fibrillation. The early explanation for alternans development was the voltage-driven mechanism, where the action potential (AP) restitution steepness was considered as crucial determining factor. Recent results suggest that restitution slope is an inadequate predictor for alternans development, but several studies still claim the role of membrane potential as underlying mechanism of alternans. These controversial data indicate that the relationship of restitution and alternans development is not completely understood. APs were measured by conventional microelectrode technique from canine right ventricular papillary muscles. Ionic currents combined with fluorescent measurements were recorded by patch-clamp technique. APs combined with fluorescent measurements were monitored by sharp microelectrodes. Rapid pacing evoked restitution-independent AP duration (APD) alternans. When non-alternating AP voltage command was used, Ca2+i-transient (CaT) alternans were not observed. When alternating rectangular voltage pulses were applied, CaT alternans were proportional to ICaL amplitude alternans. Selective ICaL inhibition did not influence the fast phase of APD restitution. In this study we found that ICaL has minor contribution in shaping the fast phase of restitution curve suggesting that ICaL—if it plays important role in the alternans mechanism—could be an additional factor that attenuates the reliability of APD restitution slope to predict alternans.},
	year = {2021},
	eissn = {2045-2322},
	orcid-numbers = {Horváth, Balázs/0000-0003-2562-8446; Varró, András/0000-0003-0745-3603}
}

@article{MTMT:31962151,
	title = {Omecamtiv mecarbil evokes diastolic dysfunction and leads to periodic electromechanical alternans},
	url = {https://m2.mtmt.hu/api/publication/31962151},
	author = {Fülöp, Gábor Áron and Oláh, Attila and Csípő, Tamás and Kovács, Árpád and Pórszász, Róbert and Veress, Roland and Horváth, Balázs and Nagy, László and Bódi, Beáta and Fagyas, Miklós and Helgadottir, Solveig Lind and Bánhegyi, Viktor and Juhász, Béla and Bombicz, Mariann and Priksz, Dániel and Nánási, Péter Pál and Merkely, Béla Péter and Édes, István and Csanádi, Zoltán and Papp, Zoltán and Radovits, Tamás and Tóth, Attila},
	doi = {10.1007/s00395-021-00866-8},
	journal-iso = {BASIC RES CARDIOL},
	journal = {BASIC RESEARCH IN CARDIOLOGY},
	volume = {116},
	unique-id = {31962151},
	issn = {0300-8428},
	abstract = {Omecamtiv mecarbil (OM) is a promising novel drug for improving cardiac contractility. We tested the therapeutic range of OM and identified previously unrecognized side effects. The Ca2+ sensitivity of isometric force production (pCa50) and force at low Ca2+ levels increased with OM concentration in human permeabilized cardiomyocytes. OM (1 µM) slowed the kinetics of contractions and relaxations and evoked an oscillation between normal and reduced intracellular Ca2+ transients, action potential lengths and contractions in isolated canine cardiomyocytes. Echocardiographic studies and left ventricular pressure–volume analyses demonstrated concentration-dependent improvements in cardiac systolic function at OM concentrations of 600–1200 µg/kg in rats. Administration of OM at a concentration of 1200 µg/kg was associated with hypotension, while doses of 600–1200 µg/kg were associated with the following aspects of diastolic dysfunction: decreases in E/A ratio and the maximal rate of diastolic pressure decrement (dP/dtmin) and increases in isovolumic relaxation time, left atrial diameter, the isovolumic relaxation constant Tau, left ventricular end-diastolic pressure and the slope of the end-diastolic pressure–volume relationship. Moreover, OM 1200 µg/kg frequently evoked transient electromechanical alternans in the rat in vivo in which normal systoles were followed by smaller contractions (and T-wave amplitudes) without major differences on the QRS complexes. Besides improving systolic function, OM evoked diastolic dysfunction and pulsus alternans. The narrow therapeutic window for OM may necessitate the monitoring of additional clinical safety parameters in clinical application.},
	keywords = {heart failure; diastolic dysfunction; Inotropy; Omecamtiv mecarbil; Ca2+ sensitivity; Pulsus alternans},
	year = {2021},
	eissn = {1435-1803},
	orcid-numbers = {Horváth, Balázs/0000-0003-2562-8446; Merkely, Béla Péter/0000-0001-6514-0723}
}

@article{MTMT:31804198,
	title = {The role of calcium homeostasis remodeling in inherited cardiac arrhythmia syndromes},
	url = {https://m2.mtmt.hu/api/publication/31804198},
	author = {Hamilton, Shanna and Veress, Roland and Belevych, Andriy and Terentyev, Dmitry},
	doi = {10.1007/s00424-020-02505-y},
	journal-iso = {PFLUG ARCH EUR J PHY},
	journal = {PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY},
	volume = {473},
	unique-id = {31804198},
	issn = {0031-6768},
	abstract = {Sudden cardiac death due to malignant ventricular arrhythmias remains the major cause of mortality in the postindustrial world. Defective intracellular Ca2+ homeostasis has been well established as a key contributing factor to the enhanced propensity for arrhythmia in acquired cardiac disease, such as heart failure or diabetic cardiomyopathy. More recent advances provide a strong basis to the emerging view that hereditary cardiac arrhythmia syndromes are accompanied by maladaptive remodeling of Ca2+ homeostasis which substantially increases arrhythmic risk. This brief review will focus on functional changes in elements of Ca2+ handling machinery in cardiomyocytes that occur secondary to genetic mutations associated with catecholaminergic polymorphic ventricular tachycardia, and long QT syndrome.},
	keywords = {heart failure; LONG QT SYNDROME; catecholaminergic polymorphic ventricular tachycardia; Calcium-dependent arrhythmia; Calcium homeostasis remodeling},
	year = {2021},
	eissn = {1432-2013},
	pages = {377-387}
}

@article{MTMT:31795546,
	title = {Blockade of sodium‑calcium exchanger via ORM-10962 attenuates cardiac alternans},
	url = {https://m2.mtmt.hu/api/publication/31795546},
	author = {Szlovák, Jozefina and Tomek, Jakub and Zhou, Xin and Tóth, Noémi and Veress, Roland and Horváth, Balázs and Szentandrássy, Norbert and Levijoki, Jouko and Papp, Gyula and Herring, Neil and Varró, András and Eisner, David A and Rodriguez, Blanca and Nagy, Norbert},
	doi = {10.1016/j.yjmcc.2020.12.015},
	journal-iso = {J MOL CELL CARDIOL},
	journal = {JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY},
	volume = {153},
	unique-id = {31795546},
	issn = {0022-2828},
	abstract = {Repolarization alternans, a periodic oscillation of long-short action potential duration, is an important source of arrhythmogenic substrate, although the mechanisms driving it are insufficiently understood. Despite its relevance as an arrhythmia precursor, there are no successful therapies able to target it specifically. We hypothesized that blockade of the sodium‑calcium exchanger (NCX) could inhibit alternans. The effects of the selective NCX blocker ORM-10962 were evaluated on action potentials measured with microelectrodes from canine papillary muscle preparations, and calcium transients measured using Fluo4-AM from isolated ventricular myocytes paced to evoke alternans. Computer simulations were used to obtain insight into the drug's mechanisms of action. ORM-10962 attenuated cardiac alternans, both in action potential duration and calcium transient amplitude. Three morphological types of alternans were observed, with differential response to ORM-10962 with regards to APD alternans attenuation. Analysis of APD restitution indicates that calcium oscillations underlie alternans formation. Furthermore, ORM-10962 did not markedly alter APD restitution, but increased post-repolarization refractoriness, which may be mediated by indirectly reduced L-type calcium current. Computer simulations reproduced alternans attenuation via ORM-10962, suggesting that it is acts by reducing sarcoplasmic reticulum release refractoriness. This results from the ORM-10962-induced sodium‑calcium exchanger block accompanied by an indirect reduction in L-type calcium current. Using a computer model of a heart failure cell, we furthermore demonstrate that the anti-alternans effect holds also for this disease, in which the risk of alternans is elevated. Targeting NCX may therefore be a useful anti-arrhythmic strategy to specifically prevent calcium driven alternans.},
	keywords = {SODIUM-CALCIUM EXCHANGER; Canine myocytes; alternans; Cardiac simulation; Sodium‑calcium exchanger inhibition},
	year = {2021},
	eissn = {1095-8584},
	pages = {111-122},
	orcid-numbers = {Horváth, Balázs/0000-0003-2562-8446; Szentandrássy, Norbert/0000-0003-0197-9567; Varró, András/0000-0003-0745-3603}
}

@article{MTMT:32025835,
	title = {Late sodium current in human, canine and guinea pig ventricular myocardium},
	url = {https://m2.mtmt.hu/api/publication/32025835},
	author = {Horváth, Balázs and Hézső, Tamás and Szentandrássy, Norbert and Kistamás, Kornél and Árpádffy-Lovas, Tamás and Varga, Richárd Sándor and Gazdag, Péter and Veress, Roland and Dienes, Csaba Bálint and Baranyai, Dóra and Almássy, János and Virág, László and Nagy, Norbert and Baczkó, István and Magyar, János and Bányász, Tamás and Varró, András and Nánási, Péter Pál},
	doi = {10.1016/j.yjmcc.2019.12.015},
	journal-iso = {J MOL CELL CARDIOL},
	journal = {JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY},
	volume = {139},
	unique-id = {32025835},
	issn = {0022-2828},
	abstract = {Although late sodium current (INa-late) has long been known to contribute to plateau formation of mammalian cardiac action potentials, lately it was considered as possible target for antiarrhythmic drugs. However, many aspects of this current are still poorly understood. The present work was designed to study the true profile of INa-late in canine and guinea pig ventricular cells and compare them to INa-late recorded in undiseased human hearts. INa-late was defined as a tetrodotoxin-sensitive current, recorded under action potential voltage clamp conditions using either canonic- or self-action potentials as command signals. Under action potential voltage clamp conditions the amplitude of canine and human INa-late monotonically decreased during the plateau (decrescendo-profile), in contrast to guinea pig, where its amplitude increased during the plateau (crescendo profile). The decrescendo-profile of canine INa-late could not be converted to a crescendo-morphology by application of ramp-like command voltages or command action potentials recorded from guinea pig cells. Conventional voltage clamp experiments revealed that the crescendo INa-late profile in guinea pig was due to the slower decay of INa-late in this species. When action potentials were recorded from multicellular ventricular preparations with sharp microelectrode, action potentials were shortened by tetrodotoxin, which effect was the largest in human, while smaller in canine, and the smallest in guinea pig preparations. It is concluded that important interspecies differences exist in the behavior of INa-late. At present canine myocytes seem to represent the best model of human ventricular cells regarding the properties of INa-late. These results should be taken into account when pharmacological studies with INa-late are interpreted and extrapolated to human. Accordingly, canine ventricular tissues or myocytes are suggested for pharmacological studies with INa-late inhibitors or modifiers. Incorporation of present data to human action potential models may yield a better understanding of the role of INa-late in action potential morphology, arrhythmogenesis, and intracellular calcium dynamics.},
	keywords = {Dogs; Animals; Adult; Female; Male; Humans; metabolism; MYOCARDIUM; ARTICLE; PATHOPHYSIOLOGY; ION CHANNELS; CA2+ CHANNELS; human; animal; Guinea Pigs; priority journal; controlled study; MYOCYTES; dog; nonhuman; animal experiment; animal cell; species difference; drug effect; tetrodotoxin; Sodium Channels; sodium channel; Action Potentials; action potential; Heart Ventricles; human cell; ventricular repolarization; Guinea pig; Ion Channel Gating; Myocytes, Cardiac; action potential duration; heart depolarization; cardiac muscle; heart ventricle; channel gating; heart repolarization; sodium current; Dog myocytes; repolarization reserve; LATE NA+ CURRENT; heart muscle fiber membrane potential; Cardiac & Cardiovascular Systems; cardiac muscle cell; voltage clamp technique; Cnidarian Venoms; K+ CURRENTS; mongrel dog; coelenterate venom; toxin II (Anemonia sulcata); action potential voltage clamp; action potential voltage clamp; Human myocytes; conventional voltage clamp; VOLTAGE-DEPENDENT BLOCK},
	year = {2020},
	eissn = {1095-8584},
	pages = {14-23},
	orcid-numbers = {Horváth, Balázs/0000-0003-2562-8446; Szentandrássy, Norbert/0000-0003-0197-9567; Baczkó, István/0000-0002-9588-0797; Varró, András/0000-0003-0745-3603}
}

@article{MTMT:31975038,
	title = {Az akciós potenciál alatt létrejövő késői nátriumáram tulajdonságai tengerimalac, kutya, illetve humán balkamrai szívizomsejtekben = Late sodium current in canine, guinea pig and human ventricular myocardium},
	url = {https://m2.mtmt.hu/api/publication/31975038},
	author = {Dienes, Csaba Bálint and Horváth, Balázs and Hézső, Tamás and Szentandrássy, Norbert and Kistamás, Kornél and Árpádffy-Lovas, Tamás and Varga, Richárd Sándor and Veress, Roland and Kiss, Dénes Zsolt and Baranyai, Dóra and Almássy, János and Virág, László and Nagy, Norbert and Baczkó, István and Magyar, János and Bányász, Tamás and Varró, András and Nánási, Péter Pál},
	journal-iso = {CARDIOL HUNG},
	journal = {CARDIOLOGIA HUNGARICA},
	volume = {50},
	unique-id = {31975038},
	issn = {0133-5596},
	year = {2020},
	eissn = {1588-0230},
	pages = {176-176},
	orcid-numbers = {Horváth, Balázs/0000-0003-2562-8446; Szentandrássy, Norbert/0000-0003-0197-9567; Baczkó, István/0000-0002-9588-0797; Varró, András/0000-0003-0745-3603}
}

@article{MTMT:31357281,
	title = {Regulation of the delayed rectifier potassium current during the adrenergic adaptation of cardiomyocytes},
	url = {https://m2.mtmt.hu/api/publication/31357281},
	author = {Kiss, Dénes Zsolt and Hézső, Tamás and Kurtan, B and Veress, Roland and Baranyai, Dóra and Kovacs, Z S and Dienes, Csaba Bálint and Szentandrássy, Norbert and Bányász, Tamás and Magyar, János and Nánási, Péter Pál and Horváth, Balázs},
	doi = {10.1093/europace/euaa162.191},
	journal-iso = {EUROPACE},
	journal = {EUROPACE},
	volume = {22},
	unique-id = {31357281},
	issn = {1099-5129},
	year = {2020},
	eissn = {1532-2092},
	orcid-numbers = {Horváth, Balázs/0000-0003-2562-8446}
}