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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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DOI
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2.

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)
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3.

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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