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1.

001-es BibID:BIBFORM041490
035-os BibID:(Wos)000251331300008 (Scopus)36349018414
Első szerző:Brugós László (tüdőgyógyász, klinikai immunológus, allergológus)
Cím:Modulation of adenosine-induced response in the guinea pig trachea duirng long-term caffeine treatment : possible role of epthelium / László Brugós, Rudolf Gesztelyi, Judit Zsuga, Ágnes Cseppentő, Ilona Benkő, Zoltán Galajda, György Deák, Sándor Sipka, Tamás Rőszer, Péter Kovács, Mária Szilasi, István Édes, András József Szentmiklósi
Dátum:2007
ISSN:1347-8613
Megjegyzések:The responses to adenosine were studied on isolated, methacholine-precontracted tracheal strips of guinea pigs in the course of long-term caffeine or solvent treatment. Guinea pigs were fed caffeine for 10 weeks (average serum caffeine concentration: 39.1 ± 3.9 ?M). In epithelium-intact tracheal preparations (EITPs), sensititization to adenosine-induced relaxation (AIR) developed. It attained a maximum in week 1 of caffeine treatment, and then its level diminished and disappeared completely by weeks 4 - 6. In epithelium-denuded tracheal preparations (EDTPs), an increase in the sensitivity to adenosine was observed from week 1 to week 10 (a 4 - 6-fold reduction in EC50). Use of a coaxial bioassay system confirmed the role of epithelium in this process. The enhancement of the AIR of the EITPs was not modified by inhibitors of cyclooxygenase and lipoxygenase. Following depletion of the neuropeptides by acute capsaicin pretreatment, the AIR of the EITPs was strongly enhanced after caffeine treatment for 6 weeks. In chronically caffeine-treated EITPs, the inhibition of neutral endopeptidase led to dramatic reduction of the AIR. On the basis of the results by inhibiting nitric oxide synthase, it can be supposed that nitric oxide released from EITPs of long-lasting caffeine-treated animals operated as a constrictor agent. Our results show that chronic caffeine treatment gives rise to an initial sensitization to adenosine of the EITPs, this being followed by the development of a specific adaptive process in the epithelial cells, which counterbalances the increased tracheal sensitivity to adenosine.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Journal Of Pharmacological Sciences. - 105 : 3 (2007), p. 279-290. -
További szerzők:Gesztelyi Rudolf (1969-) (kísérletes farmakológus) Zsuga Judit (1973-) (neurológus, pszichoterapeuta, egészségügyi szakmanager) Cseppentő Ágnes (1953-) (orvos) Benkő Ilona (1954-) (orvos, farmakológus) Galajda Zoltán (1962-) (szívsebész, érsebész) Deák György (1954-) (polimer kémikus) Sipka Sándor (1945-) (laboratóriumi szakorvos) Röszer Tamás (1979-) (orvos, biológus) Kovács Péter (1939-) (farmakológus) Szilasi Mária (1953-) (tüdőgyógyász, klinikai immunológus, allergológus, belgyógyász) Édes István (1952-) (kardiológus) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos)
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2.

001-es BibID:bibKLT00004875
Első szerző:Cseppentő Ágnes (orvos)
Cím:Long-lasting treatment with adenosine receptor antagonists : effects on hypoxic tolerance and vascular responsiveness / Á. Cseppentő, A. Ujfalusi, K. Antal, J. Szegi, J. Zs. Szabó, P. Kovács, A. J. Szentmiklósi
Dátum:1996
ISSN:0231-424X
Megjegyzések:In electrically driven myocardial preparations obtained from chronically methylxanthine-[aminophylline (APH) and 8-phenyltheophylline (8-PT)] or solvent(DMSO)-treated guinea pigs no differences were found in alteration of mechanical activity under hypoxia and reoxygenation. The vasoconstrictor effects observed after in vitro exposure of pulmonary arterial preparations (excised from either methylxanthine- or solvent-treated guinea pigs) to both noradrenaline and PGF2 alpha were also similar. In methylxanthine-treated vascular tissues, however, nitroglycerin and NO exerted more pronounced vasorelaxant effect than in specimens prepared from solvent-treated guinea pigs
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény hazai lapban
folyóiratcikk
Megjelenés:Acta Physiologica Hungarica. - 84 : 3 (1996), p. 275-276. -
További szerzők:Ujfalusi Anikó (1968-) (gyermekorvos, laboratóriumi szakorvos) Antal Károly (1956-) (kémikus) Szegi József (1926-2001) (gyógyszerész) Szabó Judit Zsuzsanna (farmakológus, klinikai laboratóriumi szakorvos) Kovács Péter (1939-) (farmakológus) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos)
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3.

001-es BibID:BIBFORM015066
035-os BibID:(WOS)000297855700007 (Scopus)82455174750
Első szerző:Galajda Zoltán (szívsebész, érsebész)
Cím:Histamine and H1-Histamine receptors faster venous circulation / Zoltan Galajda, Jozsef Balla, A. Jozsef Szentmiklosi, Tamas Biro, Gabriella Czifra, Nora Dobrosi, Agnes Cseppento, Lajos Patonay, Tamas Roszer, Gyorgy Balla, Laurenciu M. Popescu, Istvan Lekli, Arpad Tosaki
Dátum:2011
Megjegyzések:The study has analysed the action of histamine in the rabbit venous system and evaluated its potential role in contraction during increased venous pressure. We have found that a great variety exists in histamine sensitivity and H1-histamine receptor expression in various types of rabbit veins. Veins of the extremities (saphenous vein, femoral vein, axillary vein) and abdomen (common iliac vein, inferior vena cava) responded to histamine by a prominent, concentration-dependent force generation, whereas great thoracic veins (subclavian vein, superior vena cavas, intrathoracic part of inferior vena cava) and a pelvic vein (external iliac vein) exhibited slight sensitivity to exogenous histamine. The lack of reactivity to histamine was not due to increased activity of nitric oxide synthase (NOS) or heme oxygenase-1. H1-histamine receptor expression of veins correlated well with the histamine-induced contractions. Voltage-dependent calcium channels mediated mainly the histamine-induced force generation of saphenous vein, whereas it did not act in the inferior vena cava. In contrast, the receptor-operated channels were not involved in this response in either vein. Tyrosine phosphorylation occurred markedly in response to histamine in the saphenous vein, but not in the inferior vena cava. Histamine induced a prominent p kinase activation in both vessels. Protein kinase C and mitogen-activated protein kinase (MAPK) were not implicated in the histamine-induced intracellular calcium sensitization. Importantly, transient clamping of the femoral vein in animals caused a short-term constriction, which was inhibited by H1-histamine receptor antagonist in vivo. Furthermore, a significantly greater histamine immunopositivity was detected in veins after stretching compared to the resting state. We conclude that histamine receptor density adapts to the actual requirements of the circulation, and histamine liberated by the venous wall during increased venous pressure contributes to the contraction of vessels, providing a force for the venous return.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Molekuláris Medicina
Megjelenés:Journal of Cellular and Molecular Medicine. - 15 : 12 (2011), p. 2614-2623. -
További szerzők:Balla József (1959-) (belgyógyász, nephrológus) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Bíró Tamás (1968-) (élettanász) Czifra Gabriella (1975-) (élettanász) Dobrosi Nóra (1981-) (molekuláris biológus) Cseppentő Ágnes (1953-) (orvos) Patonay Lajos (anatómus) Röszer Tamás (1979-) (orvos, biológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Popescu, Laurenciu M. Lekli István (1981-) (gyógyszerész) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Vaszkuláris biológia
K-72315
OTKA
TÁMOP 4.2.2-08/1-2008-0007
TÁMOP
ETT 586/2006
EGYÉB
ETT 147/2009
EGYÉB
K 75883
OTKA
K 83478
OTKA
MTA-DE-11003
EGYÉB
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4.

001-es BibID:BIBFORM057912
Első szerző:Gesztelyi Rudolf (kísérletes farmakológus)
Cím:Positive inotropic effect of the inhibition of cyclic GMP-stimulated 3',5'-cyclic nucleotide phosphodiesterase (PDE2) on guinea pig left atria in eu- and hyperthyroidism / R. Gesztelyi, J. Zsuga, P. Hajdú, J. Zs. Szabó, A. Cseppentő, A. J. Szentmiklósi
Dátum:2003
ISSN:0231-5882
Megjegyzések:The significance of PDE2 on the atrial inotropy was studied in eu- and hyperthyroidism. The contractile force was measured and negative inotropic capacity of N6-cyclopentyladenosine (CPA) was determined on left atria isolated from 8-day thyroxine- or solvent-treated guinea pigs, in the presence or absence of EHNA (adenosine deaminase and PDE2 inhibitor) or NBTI (nucleoside transporter inhibitor). EHNA was administered to inhibit PDE2, while NBTI was used to model the accumulation of endogenous adenosine. The reduction of the contractile force caused by EHNA was smaller in the thyroxine-treated atria than in the solvent-treated samples. Contrary, NBTI induced a decrease in the contractile force without significant difference between the two groups. In addition, EHNA enhanced the efficiency of CPA in thyroxine-treated atria and did not affect it in solvent-treated samples, while the response to CPA was decreased by NBTI in all atria, especially in hyperthyroidism. On the basis of greater retention of the contractile force and sustained/enhanced responsiveness to CPA in the presence of EHNA we conclude that PDE2's inhibition has a significant positive inotropic effect in guinea pig atria and this effect is proven to be augmented in hyperthyroidism.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:General Physiology and Biophysics. - 22 : 4 (2003), p. 501-513. -
További szerzők:Zsuga Judit (1973-) (neurológus, pszichoterapeuta, egészségügyi szakmanager) Hajdu Péter (1975-) (biofizikus) Szabó Judit Zsuzsanna (farmakológus, klinikai laboratóriumi szakorvos) Cseppentő Ágnes (1953-) (orvos) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos)
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5.

001-es BibID:BIBFORM028062
Első szerző:Gesztelyi Rudolf (kísérletes farmakológus)
Cím:Special sensitization pattern in adenosine-induced myocardial responses after thyroxine-treatment / Gesztelyi Rudolf, Zsuga Judit, Cseppentő Ágnes, Bajza Ágnes, Varga Angelika, Szabó Zs. Judit, Szentmiklósi József A.
Dátum:2003
Megjegyzések:Chronic thyroxine treatment reduces the susceptibility of atrial myocardium to adenosine. While the possible role of membrane adenosine receptors in this action is supported by several studies, the involvement of intracellular adenosine mechanisms has not been defined. The present experiments were carried out in electrically driven euthyroid and hyperthyroid guinea pig atrial myocardium. The extracellular and intracellular actions of adenosine were analyzed pharmacologically by the use of specific blockers of membrane adenosine transport and intracellular adenosine deaminase (ADA). The involvement of phosphoprotein phosphatase, phospholamban, and sarcoplasmic reticulum Ca2+ ATPase (SERCA) in the adenosine-induced responses was also studied. The major findings were as follows: i) pD(2)- and E(max)-values for adenosine-induced decrease of mechanical activity were significantly reduced after an 8-day thyroxine treatment in atrial tissues; ii) in atria of thyroxine-treated animals, membrane purine transport inhibitors (dipyridamole, NBTI) induced similar leftward shifts in concentration-response curves for adenosine in both euthyroid and hyperthyroid atrial myocardium without altering the depressed E(max) values; iii) the leftward displacement evoked by inhibitors of intracellularly located ADA (coformycin, EHNA) was more striking in hyperthyroid than euthyroid myocardia. ADA inhibitors induced a complete reversal of the maximum adenosine actions; iv) inhibition by cantharidin of phosphoprotein phosphatases (after inhibition of ADA) reduced the adenosine-induced responses. This inhibition was stronger in hyperthyroid atria; v) pharmacological elimination of sarcoplasmic reticulum Ca2+ ATPase by cyclopiazonic acid did not alter the cardiac responses to adenosine and this was independent of thyroid status. It is suggested that distinct modulation of the extra- and intracellular adenosine actions is present in eu- and hyperthyroid hearts. In the latter, a predominance of intracellular adenosine mechanisms can be proposed.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of pharmacological sciences 91 : 4 (2003), p. 295-304. -
További szerzők:Zsuga Judit (1973-) (neurológus, pszichoterapeuta, egészségügyi szakmanager) Cseppentő Ágnes (1953-) (orvos) Bajza Ágnes (1970-) (biológus) Varga Angelika (1977-) (biológus) Szabó Judit Zsuzsanna (farmakológus, klinikai laboratóriumi szakorvos) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos)
Internet cím:DOI
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6.

001-es BibID:BIBFORM046089
Első szerző:Rubovszky Bálint (élettanász)
Cím:Comparative pharmacological studies on the A2 adenosine receptor agonist 5'-n-ethyl-carboxamidoadenosine and its F19 isotope labelled derivative / Rubovszky B., Szentmiklosi A. J., Marian T., Cseppento A., Gesztelyi R., Szekely A., Forizs F., Gaspar R., Tron L., Krasznai Z.
Dátum:2003
ISSN:1347-8613
Megjegyzések:Adenosine receptors are expressed in various mammalian tissues where they mediate the effects of adenosine on cellular functions through a number of signalling mechanisms. 18F-NECA is the positron-emitting derivative of the A(2)-receptor agonist NECA (5'-n-ethyl-carboxamidoadenosine) and is a radioligand for PET imaging of adenosine receptors. Contractility and relaxation studies were performed on guinea pig atrial myocardium, pulmonary artery, and thoracic aorta to compare the pharmacological effects of NECA and F-NECA (a non-emitting derivative) on tissues. Furthermore, the effect of NECA and F-NECA on the potassium conductance was investigated in DDT1 MF-2 smooth muscle cells with the patch-clamp technique. Both NECA and F-NECA reduced the contractile force in atrial myocardium and evoked phasic contraction in pulmonary artery (A(1) adenosine-receptor-mediated actions) in a dose dependent manner; however, the apparent affinity was lower for F-NECA. No difference was found in relaxation induced by these compounds in 1 microM noradrenaline-precontracted aorta and pulmonary artery (in the presence of DPCPX, an A(1) adenosine receptor antagonist, tissue containing A(2B) adenosine receptors). NECA (5 microM) and F-NECA (5 microM) also decreased the peak current and accelerated activation and inactivation properties of the potassium channels, but F-NECA was less effective. These results suggest that while NECA and F-NECA are equivalent agonists of vascular A(2B) receptors, they mediate different changes of some parameters. When evaluating the data obtained by the use of radiolabelled ligands, one has to take into consideration the possible physiological effects of the ligands besides its binding properties to tissues.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Pharmacological Sciences. - 93 : 3 (2003), p. 356-363. -
További szerzők:Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Márián Teréz (1950-) (radiobiológus) Cseppentő Ágnes (1953-) (orvos) Gesztelyi Rudolf (1969-) (kísérletes farmakológus) Székely Andrea Forizs Fruzsina Gáspár Rezső (1944-) (biofizikus) Trón Lajos (1941-) (biofizikus) Krasznai Zoltán (1950-) (biofizikus)
Pályázati támogatás:T 043087
OTKA
T 038270
OTKA
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7.

001-es BibID:BIBFORM056739
Első szerző:Szentmiklósi József András (farmakológus, klinikai laboratóriumi szakorvos)
Cím:The janus face of adenosine : antiarrhythmic and proarrhythmic actions / A. József Szentmiklósi, Zoltán Galajda, Ágnes Cseppentő, Rudolf Gesztelyi, Zsolt Susán, Bence Hegyi, Péter P. Nánási
Dátum:2015
ISSN:1381-6128
Megjegyzések:Adenosine is a ubiquitous, endogenous purine involved in a variety of physiological and pathophysiological regulatory mechanisms. Adenosine has been proposed as an endogenous antiarrhythmic substance to prevent hypoxia/ischemia-induced arrhythmias. Adenosine (and its precursor, ATP) has been used in the therapy of various cardiac arrhythmias over the past six decades. Its primary indication is treatment of paroxysmal supraventricular tachycardia, but it can be effective in other forms of supraventricular and ventricular arrhythmias, like sinus node reentry based tachycardia, triggered atrial tachycardia, atrioventricular nodal reentry tachycardia, or ventricular tachycardia based on a cAMP-mediated triggered activity. The main advantage is the rapid onset and the short half life (1- 10 sec). Adenosine exerts its antiarrhythmic actions by activation of A1 adenosine receptors located in the sinoatrial and atrioventricular nodes, as well as in activated ventricular myocardium. However, adenosine can also elicit A2A, A2B and A3 adenosine receptor-mediated global side reactions (flushing, dyspnea, chest discomfort), but it may display also proarrhythmic actions mediated by primarily A1 adenosine receptors (e.g. bradyarrhythmia or atrial fibrillation). To avoid the non-specific global adverse reactions, A1 adenosine receptor- selective full agonists (tecadenoson, selodenoson, trabodenoson) have been developed, which agents are currently under clinical trial. During long-term administration with orthosteric agonists, adenosine receptors can be internalized and desensitized. To avoid desensitization, proarrhythmic actions, or global adverse reactions, partial A1 adenosine receptor agonists, like CVT-2759, were developed. In addition, the pharmacologically "silent" site- and event specific adenosinergic drugs, such as adenosine regulating agents and allosteric modulators, might provide attractive opportunity to increase the effectiveness of beneficial actions of adenosine and avoid the adverse reactions.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Adenosinergic drugs
antiarrhythmic action
proarrhythmic effect
adenosine A1 receptor activators
partial A1 adenosine receptor agonists
adenosine regulators
allosteric receptor modulators
drug development
Megjelenés:Current Pharmaceutical Design. - 21 : 8 (2015), p. 965-976. -
További szerzők:Galajda Zoltán (1962-) (szívsebész, érsebész) Cseppentő Ágnes (1953-) (orvos) Gesztelyi Rudolf (1969-) (kísérletes farmakológus) Susán Zsolt (1983-) (sebész) Hegyi Bence (1987-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Sebészet Kutatócsoport
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8.

001-es BibID:BIBFORM020347
035-os BibID:WOS:000294414700008
Első szerző:Szentmiklósi József András (farmakológus, klinikai laboratóriumi szakorvos)
Cím:Xanthine derivatives in the heart : blessed or cursed? / Szentmiklosi A. J., Cseppento A., Gesztelyi R., Zsuga J., Kortvely A., Harmati G., Nanasi P. P.
Dátum:2011
ISSN:0929-8673
Megjegyzések:Methylxanthines, such as theophylline, have been used to treat cardiorespiratory disorders, whereas caffeine is the most widely consumed psychoactive agent in various soft drinks. Because of the worldwide use of these drugs and the recently synthesized xanthine derivatives, an intensive research on the cardiac actions of these substances is under progress. This review focuses on the molecular mechanisms involved in the actions of xanthine derivatives with special reference to their adenosine receptor antagonistic properties. The main basic and human studies on the action of xanthines on impulse initiation and conduction, as well as the electrophysiological and mechanical activity of the working myocardium will be overviewed. The potential beneficial and harmful actions of the methylxanthines will be discussed in light of the recent experimental and clinical findings. The pharmacological features and clinical observations with adenosine receptor subtype-specific xanthine antagonists are also the subject of this paper. Based on the adenosine receptor-antagonistic activity of these compounds, it can be raised that xanthine derivatives might inhibit the cardioprotective action of endogenous adenosine on various subtypes (A(1), A(2A), A(2B) and A(3)) of adenosine receptors. Adenosine is an important endogenous substance with crucial role in the regulation of cardiac function under physiological and pathological conditions (preconditioning, postconditioning, ischemia/reperfusion injury). Recent clinical studies show that acute administration of caffeine or theophylline can inhibit various types of preconditioning in human subjects. There are no human studies, however, for the cardiovascular actions of long-term administration of these drugs. Upregulation of adenosine receptors and increased effectiveness of adenosine receptor-related cardiovascular functions have been observed after long-lasting treatment with methylxanthines. In addition, there are data indicating that blood adenosine level increases after long-term caffeine administration. Since the salutary actions (and also the adverse reactions) of a number of xanthine derivatives are repeatedly shown, the main goal is the development of novel structures that mimic the actions of the conventional methylxanthines as lead compounds, but their adenosine receptor subtype-specificity is higher, their water solubility is optimal, and the unwanted reactions are minimized.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Current Medicinal Chemistry. - 18 : 24 (2011), p. 3695-3706. -
További szerzők:Cseppentő Ágnes (1953-) (orvos) Gesztelyi Rudolf (1969-) (kísérletes farmakológus) Zsuga Judit (1973-) (neurológus, pszichoterapeuta, egészségügyi szakmanager) Körtvély Ágnes Harmati Gábor (1983-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

9.

001-es BibID:BIBFORM016601
Első szerző:Szentmiklósi József András (farmakológus, klinikai laboratóriumi szakorvos)
Cím:Novel trends in the treatment of cardiovascular disorders : site- and event- selective adenosinergic drugs. / Szentmiklósi A. J., Cseppento A., Harmati G., Nánási P. P.
Dátum:2011
ISSN:0929-8673
Megjegyzések:This review focuses on the potential role of site- and event-selective adenosinergic drugs in the treatment of cardiovascular diseases. Adenosine is released from the myocardium and vessels in response to various forms of stress and acts on four receptor subtypes (A1, A2A, A2B and A3). Adenosine is an important endogenous substance with important homeostatic activity in the regulation of cardiac function and circulation. Adenosine receptors are also involved in the modulation of various cellular events playing crucial role in physiological and pathological processes of the cardiovascular system. These actions are associated to activation of distinct adenosine receptor subtypes, therefore drugs targeting specific adenosine receptors might be promising therapeutic tools in treatment of several disorders including various forms of cardiac arrhythmia, myocardial ischemia-reperfusion injury, angina pectoris, chronic heart failure, etc. Recently, in addition to subtype-specific adenosine receptor agonists and antagonists, a number of substances that enhance adenosine receptor activation locally at the site where the release of endogenous adenosine is the most intensive have been developed. Thus global actions of adenosine receptor agonists and antagonists, as well as desensitization or down-regulation following chronic administration of these orthosteric compounds can possibly be avoided. We discuss the chemical, pharmacological and clinical features of these compounds: (1) inhibitors of membrane adenosine transporters (NBTI, dipyridamole), (2) inhibitors of adenosine deaminase (coformycin, EHNA), (3) inhibitors of adenosine kinase (tubercidin, aristeromycin), (4) inhibitors of AMP deaminase (GP3269), (5) activators of 5'- nucleotidase (methotrexate), (6) adenosine regulators (acadesine) and (7) allosteric adenosine receptor modulators (PD81723, LUF6000). The development of this type of substances might offer a novel therapeutic approach for treating cardiovascular diseases in the near future.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Site and event specific action
adenosinergic drugs
membrane adenosine transport
adenosine deaminase
adenosine kinase
AMP deaminase
5'-nucleotidase
adenosine regulators
allosteric receptor modulators
Megjelenés:Current Medicinal Chemistry. - 18 : 8 (2011), p. 1164-1187. -
További szerzők:Cseppentő Ágnes (1953-) (orvos) Harmati Gábor (1983-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

10.

001-es BibID:BIBFORM009644
Első szerző:Szentmiklósi József András (farmakológus, klinikai laboratóriumi szakorvos)
Cím:Adenosine receptors mediate both contractile and relaxant effects of adenosine in main pulmonary artery of guinea pigs / Szentmiklósi A. J., Ujfalusi A., Cseppentő Á., Kovács P., Szabó J. Zs.
Dátum:1995
Megjegyzések:In guinea pig main pulmonary artery precontracted with noradrenaline, adenosine exerted an initial phasic contraction followed by a tonic contraction and a slow relaxation. After selective blockade by 1,3-dipropyl-8-cyclopentylxanthine (DPCPX: 10 nM) of A1 receptors, adenosine only elicited a rapid relaxation. This initial response was characterized by use of adenosine (AR) and its analogues N6-cyclopentyl-adenosine (CPA), R-N6-phenylisopropyladenosine (R-PIA), 2-chloroadenosine (CADO), 5'-N-ethyl-carboxamidoadenosine(NECA), N6-2-(4-aminophenyl) ethyl adenosine (APNEA) and 2-p-((carboxyethyl)-phenethylamino)-5'-carboxamidoadenosine (CGS 21 680). The order of potency of the adenosine analogues for purine-induced phasic contraction was CPA > R-PIA > NECA = APNEA > AR > CGS 21 680 suggesting the involvement of activation of A1 type adenosine receptors in the contraction phase. DPCPX antagonized the CPA-induced contraction with a pA2 = 9.27 +/- 0.26, but the Schild plot slope parameter was significantly lower than unity (0.58 +/- 0.09). In contrast, in electrically driven guinea pig atrial myocardium (a tissue reported to possess A1 receptors), the DPCPX-CPA antagonism was purely competitive (pA2 = 8.95 +/- 0.06; slope = 0.93 +/- 0.06). In the presence of 300 nM DPCPX, the rank order of potency for the purine-induced fast relaxation was NECA > CADO = AR > CGS 21 680 = R-PIA > CPA. The NECA- and adenosine-induced relaxation was influenced neither by 300 nM CP 66713 (an antagonist at A2a receptors), nor by endothelial removal and inhibition of nitric oxide synthase (100 microM NG-nitro-L-arginine: L-NOARG)
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Naunyn-Schmiedeberg's Archives of Pharmacology. - 351 : 4 (1995), p. 417-425. -
További szerzők:Ujfalusi Anikó (1968-) (gyermekorvos, laboratóriumi szakorvos) Cseppentő Ágnes (1953-) (orvos) Kovács Péter (1939-) (farmakológus) Szabó Judit Zsuzsanna (farmakológus, klinikai laboratóriumi szakorvos)
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11.

001-es BibID:bibKLT00004876
Első szerző:Szentmiklósi József András (farmakológus, klinikai laboratóriumi szakorvos)
Cím:Regulation of purinoceptors in guinea pig pulmonary artery : functional evidences / A. J. Szentmiklósi, A. Ujfalusi, Á. Cseppentő, K. Antal, P. Kovács, J. Zs. Szabó
Dátum:1996
ISSN:0231-424X
Megjegyzések:In isolated guinea pig pulmonary arteries (precontracted with 1 microM noradrenaline) N6-cyclopentyladenosine (CPA), a selective A1 adenosine receptor agonist, exerted a concentration-dependent contraction, whereas 5'-N-ethylcarboxamidoadenosine (NECA), a non-selective A1/A2 receptor agonist, in the presence of DPCPX (a highly selective A1 receptor antagonist), produced a concentration-related rapid relaxation. Pulmonary arteries obtained from guinea pigs treated with aminophylline (APH) or 8-phenyltheophylline (8-PT) for 10 consecutive days, displayed more pronounced contraction in response to CPA compared to those of solvent-treated animals. Relaxant action of NECA was, however, attenuated in arteries prepared from methylxanthine-treated guinea pigs. Opposite changes were found in vascular tissues excised from chronically dipyridamole(DP)-treated guinea pigs.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény hazai lapban
folyóiratcikk
Megjelenés:Acta physiologica Hungarica. - 84 : 3 (1996), p. 339-341. -
További szerzők:Ujfalusi Anikó (1968-) (gyermekorvos, laboratóriumi szakorvos) Cseppentő Ágnes (1953-) (orvos) Antal Károly (1956-) (kémikus) Kovács Péter (1939-) (farmakológus) Szabó Judit Zsuzsanna (farmakológus, klinikai laboratóriumi szakorvos)
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12.

001-es BibID:bibEBI00008405
Első szerző:Ujfalusi Anikó (gyermekorvos, laboratóriumi szakorvos)
Cím:Sensitization by chronic diazepam treatment of A2A adenosine receptor-mediated relaxation in rat pulmonary artery / A. Ujfalusi, Á. Cseppentő, E. Nagy, J. Zs. Szabó, P. Kovács, A. J. Szentmiklósi
Dátum:1998
Megjegyzések:The effects of a 10-day i.p. treatment of rats with diazepam on responses to subtype selective adenosine receptor agonists were studied 3 h, 2 and 8 days after termination of diazepam treatment in isolated cardiovascular tissues possessing distinct adenosine receptors. After long-lasting diazepam exposure, the relaxation elicited by the specific A2A receptor agonist CGS 21680 was enhanced in rat main pulmonary arteries (a tissue containing A2A adenosine receptors). The increased sensitivity of A2A receptors observed 3 h and 2 days after withdrawal of diazepam was completely restored by the 8th day of the wash-out period. N6-cyclopentyladenosine (CPA)-induced suppression in mechanical activity of electrically stimulated rat atrial myocardium (a tissue containing A1 adenosine receptors) was not altered following diazepam treatment. In order to reveal the possible role of inhibition of membrane adenosine transport in the effects of diazepam (a moderate inhibitor of membrane adenosine transport), the action of a 10-day treatment with dipyridamole or S-(p-nitrobenzyl)-6-thioinosine (NBTI; prototypic adenosine uptake inhibitors) was also studied. Dipyridamole or NBTI treatment, like diazepam, increased the responsiveness of rat pulmonary artery to CGS 21680, but did not influence the cardiodepressive effect of CPA in electrically driven left atrial myocardium. The CGS 21680-induced relaxations were significantly antagonized by 10 nM ZM 241385 (a selective A2A adenosine receptor antagonist) in vessels of diazepam-treated rats. The relaxation responses to verapamil were unaltered in pulmonary arteries obtained from animals chronically treated with diazepam, dipyridamole or NBTI. These results suggest that chronic diazepam treatment is able to enhance the A2A adenosine receptor-mediated vascular functions, but does not modify the responses mediated via A1 receptors of rat myocardium, where nucleoside transport inhibitory sites of membrane are of a very low density. It is possible that sensitization of A2A adenosine receptor-mediated vasorelaxation is due to a long-lasting inhibition of membrane adenosine transporter during diazepam treatment.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Life Sciences. - 64 : 2 (1998), p. PL 19-25. -
További szerzők:Cseppentő Ágnes (1953-) (orvos) Nagy Erzsébet (1949-) (szerves kémikus, műszeres analitikus) Szabó Judit Zsuzsanna (farmakológus, klinikai laboratóriumi szakorvos) Kovács Péter (1939-) (farmakológus) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos)
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