Zoltán Márton
University of Szeged
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Featured researches published by Zoltán Márton.
The Journal of Sexual Medicine | 2005
Attila Kun; István Király; János Pataricza; Zoltán Márton; Irén Krassói; András Varró; Ulf Simonsen; Julius Gy. Papp; László Pajor
INTRODUCTION In addition to nitric oxide (NO), it is thought that an endothelium-derived hyperpolarizing factor (EDHF) plays an important role in the relaxation of penile arteries. Recently, it has been shown that C-type natriuretic peptide (CNP) shows the characteristics of EDHF in systemic small arteries. AIM To investigate the mechanism involved in CNP-evoked vasodilatation and to address whether CNP is an EDHF in human penile resistance arteries. METHODS Erectile tissue was obtained in connection with transsexual operations. Intracavernous penile resistance arteries were isolated and mounted in microvascular myographs for recording of isometric tension. Membrane potential was recorded by the use of a small glass electrode inserted in the smooth muscle layer. MAIN OUTCOME MEASURE In vitro evidence for hyperpolarization and vasorelaxation induced by CNP. RESULTS Acetylcholine (ACh) and CNP hyperpolarized smooth muscle membrane potential in resting penile resistance arteries. In penile small arteries incubated with inhibitors of NO synthase and cyclooxygenase and contracted with phenylephrine, ACh and CNP evoked concentration-dependent relaxations with maximum of 56 +/- 6% and 71 +/- 6%, respectively. Addition of a combination of blockers of small- and intermediate-conductance calcium-activated K(+) channels, apamin plus charybdotoxin, respectively, and a combination thought to block the smooth muscle response of EDHF-type relaxation, barium plus ouabain, markedly reduced ACh- and CNP-evoked relaxation. Iberiotoxin, a blocker of big-conductance calcium-activated K(+) channels inhibited the vasorelaxant responses evoked by ACh and CNP. A selective natriuretic peptide receptor type C (NPR-C) agonist, C-atrial natriuretic factor(4-23) (cANF(4-23)), induced relaxations with less maximum response compared to CNP. CONCLUSION The present findings suggest that CNP possesses the characteristics of an EDHF in human penile resistance arteries. By activation of natriuretic peptide receptor type B and NPR-C receptors, CNP causes relaxation by activation, respectively, of large-conductance calcium-activated K(+) channels and Na(+)/K(+)-adenosine triphosphatase (ATPase), and barium-sensitive inward rectifier K(+) channels. Modulation of the CNP pathway opens for new treatment modalities of erectile dysfunction.
Acta Physiologica | 2008
János Pataricza; Zoltán Márton; Cs. Lengyel; Magdolna Tóth; J.Gy. Papp; András Varró; Attila Kun
Aims: Functional roles of calcium‐activated potassium channels on the mechanical activity of epicardial coronary arteries obtained from a canine model of diabetes were investigated.
Current Pharmaceutical Design | 2014
Károly Acsai; Norbert Nagy; Zoltán Márton; Kinga Oravecz; András Varró
Driven by the limitations of the traditional antiarrhythmic pharmacology, current antiarrhythmic research is trying to identify new avenues for the development of specific and safe antiarrhythmic drugs. One of the most promising approaches in this field is the amelioration of the abnormal events in cellular Ca(2+) handling originating from the dysfunction of ryanodine receptor Ca(2+) release complex (RyR), which is an inevitable key factor in the pathology of myocardial dysfunction, remodeling and arrhythmogenesis. Accordingly, both in experimental and clinical situations, inhibition of abnormal activity of RyR, regardless of being the primary cause or a consequence during the pathogenesis appears to exert beneficial effect on disease outcome, including a marked antiarrhythmic defense. Considerable amount of our knowledge in this field originates from studies using dantrolene, a human drug with RyR stabilizing effect. Our review summarizes the cardiovascular pharmacology of dantrolene and the results of its use in experimental models of cardiac diseases, which emphasize a promising perspective for the possible antiarrhythmic application of RyR inhibition in the future.
European Journal of Pharmacology | 2018
Kinga Oravecz; Anita Kormos; Andrea Gruber; Zoltán Márton; Zsófia Kohajda; Leila Mirzaei; Norbert Jost; Jouko Levijoki; Piero Pollesello; Tuula Koskelainen; Leena Otsomaa; András Tóth; Julius Gy. Papp; Péter P. Nánási; Gudrun Antoons; András Varró; Károly Acsai; Norbert Nagy
Abstract Na+/Ca2+ exchanger (NCX) is the main Ca2+ transporter in cardiac myocytes. Its inhibition could be expected to exert positive inotropic action by accumulation of cytosolic Ca2+ ([Ca2+]i). However, we have observed only a marginal positive inotropic effect upon selective inhibition of NCX, which was enhanced when forward activity was facilitated. Here we attempted to clarify the underlying mechanism of the limited inotropic action of selective NCX inhibition by a novel inhibitor ORM‐10962 on canine ventricular myocytes. 1 &mgr;M ORM‐10962 reduced the Ca2+ content of sarcoplasmic reticulum (SR) when the reverse NCX was favoured, while SR Ca2+ content was increased by ORM‐10962 under conditions favouring the forward activity, like elevation of [Ca2+]i. L‐type Ca2+ current (ICa) was not affected by 1 &mgr;M ORM‐10962 in the absence of SR Ca2+ release, while ICa was suppressed by ORM‐10962 during normal Ca2+ cycling. The apparent degree of forward NCX inhibition was dependent on the elevation of [Ca2+]i, suggesting that an increased driving force of forward NCX can also limit the accumulation of [Ca2+i]. We concluded that in healthy myocardium the possible positive inotropic potential of NCX inhibition is considerably weaker than it was expected earlier by theoretical assumptions. The underlying mechanism may involve the autoregulation of Ca2+ handling and/or the preserved inducibility of forward NCX by high [Ca2+]i. This limitation of selective NCX inhibition seen in undiseased myocardium requires further studies in failing heart, which may allow correct evaluation of the potential therapeutic value of selective NCX inhibitors in the treatment of heart failure.
Vascular Pharmacology | 2005
Zoltán Márton; János Pataricza; Irén Krassói; András Varró; Julius Gyula Papp
Current Medicinal Chemistry | 2011
Norbert Nagy; Zoltán Márton; Loránd Kiss; András Varró; Péter P. Nánási; András Tóth
Acta Physiologica Hungarica | 2004
János Pataricza; Zoltán Márton; Z. Hegedus; Irén Krassói; Attila Kun; András Varró; J. Gy. Papp
Canadian Journal of Physiology and Pharmacology | 2016
Amir Geramipour; Zsófia Kohajda; Claudia Corici; János Prorok; Zsolt Szakonyi; Kinga Oravecz; Zoltán Márton; Norbert Nagy; András Tóth; Károly Acsai; László Virág; András Varró; Norbert Jost
Archive | 2014
Károly Acsai; Kinga Oravecz; Anita Kormos; Zoltán Márton; Gyula Papp; Andras Varro
Archive | 2009
Andras Varro; Károly Acsai; István Baczkó; Péter Biliczki; Miklós Bitay; Attila Farkas; András Farkas; Ottó Hála; Norbert Jost; István Koncz; Zsolt Kormányos; Mária Kovács; Irén Krassói; Attila Kun; Csaba Lengyel; István Leprán; Zoltán Márton; Zsolt Ákos Nagy; Balázs Ördög; Gyula Papp; Rita Papp; János Pataricza; Emese Prandovszky; János Prorok; László Sághy; Viktoria Szuts; András Tóth; Szilvia Vajda; József Ványi; Ágnes Végh