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001-es BibID:BIBFORM003872
Első szerző:Almási Róbert
Cím:Actions of 3-methyl-N-oleoyldopamine, 4-methyl-N-oleoyldopamine and N-oleoylethanolamide on the rat TRPV1 receptor in vitro and in vivo / Róbert Almási, Éva Szőke, Kata Bölcskei, Angelika Varga, Zsuzsanna Riedl
Dátum:2008
ISSN:0024-3205
Megjegyzések:N-oleoyldopamine (OLDA) has been identified as an agonist of the transient receptor potential vanilloid type 1 (TRPV1) receptor. A related fatty acid amide, N-oleoylethanolamide (OEA), was found to excite sensory neurons and produce visceral hyperalgesia via activation of the TRPV1 receptor, however, a recent study described this agent as an antinociceptive one. The aim of the present paper was to characterize two newly synthesized derivatives of N-oleoyldopamine, 3-methyl-N-oleoyldopamine (3-MOLDA) and 4-methyl-N-oleoyldopamine (4-MOLDA) as well as OEA with regard to their effects on the TRPV1 receptor. Radioactive 45Ca2+ uptake was measured in HT5-1 cells transfected with the rat TRPV1 receptor and intracellular Ca2+ concentration was monitored by fura-2 microfluorimetry in cultured trigeminal sensory neurons. Thermonociception was assessed by determining the behavioral noxious heat threshold in rats. 3-MOLDA induced 45Ca2+ uptake in a concentration-dependent manner, whereas 4-MOLDA and OEAwere without effect. 4-MOLDA and OEA, however, concentration-dependently reduced the 45Ca2+ uptake-inducing effect of capsaicin. In trigeminal sensory neurons, 3-MOLDA caused an increase in intracellular Ca2+ concentration and this effect exhibited tachyphylaxis upon repeated application. Again, 4-MOLDA and OEA failed to alter intracellular Ca2+ levels. Upon intraplantar injection, 3-MOLDA caused an 8?10 ?C drop of the noxious heat threshold in rats which was inhibited by the TRPV1 receptor antagonist iodo-resiniferatoxin. 4-MOLDA and OEA failed to alter the heat threshold but inhibited the threshold drop induced by the TRPV1 receptor agonist resiniferatoxin. These data show that 3-MOLDA behaves as an agonist, whereas 4-MOLDA and OEA appear to be antagonists, at the rat TRPV1 receptor.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
TRPV1 receptor
3-methyl-N-oleoyldopamine
4-methyl-N-oleoyldopamine
N-oleoylethanolamide
anandamide
45Ca2+ uptake
Ca2+ imaging
Increasingtemperature
Megjelenés:Life Sciences. - 82 : 11-12 (2008), p. 644-651. -
További szerzők:Szőke Éva Bölcskei Kata Varga Angelika (1977-) (biológus) Riedl Zsuzsanna
Internet cím:elektronikus változat
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2.

001-es BibID:BIBFORM030267
Első szerző:Körtvély Ágnes
Cím:Cardiovascular effects of BRX-005 comparison to bimoclomol / Ágnes Körtvély, Gyula Szigeti, Rudolf Gesztelyi, Judit Zsuga, Tamás Bányász, János Magyar, Péter Szigligeti, László Kovács, Andrea Jednákovits, A. József Szentmiklósi, Péter P. Nánási
Dátum:2000
ISSN:0024-3205
Megjegyzések:Concentration-dependent effects of BRX-005, the novel heat shock protein coinducer, cardioprotective and vasoprotective agent, on intracellular calcium transients and contractility were studied in Langendorff-perfused guinea pig hearts loaded with the fluorescent calcium indicator dye Fura-2. BRX-005 increased peak left ventricular pressure, the rate of force development and relaxation significantly in a concentration-dependent manner. The amplitude of [Ca2+](i) transients was left unaltered by the drug, in contrast to BRX-005, bimoclomol increased both contractility and the amplitude of [Ca2+](i) transients, In canine ventricular cardiomyocytes high concentrations of BRX-005 had no effect on depolarization, whereas bimoclomol suppressed action potential upstroke markedly. In guinea pig pulmonary artery preparations precontracted with phenylephrine, BRX-005 induced concentration-dependent relaxation. This effect of BRX-005 was independent of the integrity of endothelium indicating that vasorelaxant effect of the drug develops directly on vascular smooth muscle, (C) 2000 Elsevier Science Inc. All rights reserved.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Life Sciences. - 67 : 14 (2000), p. 1783-1789. -
További szerzők:Szigeti Gyula (1969-) (élettanász, elektrofiziológus) Gesztelyi Rudolf (1969-) (kísérletes farmakológus) Zsuga Judit (1973-) (neurológus, pszichoterapeuta, egészségügyi szakmanager) Bányász Tamás (1960-) (élettanász) Magyar János (1961-) (élettanász) Szigligeti Péter Kovács László (1939-) (élettanász) Jednákovits Andrea Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Nánási Péter Pál (1956-) (élettanász)
Internet cím:DOI
elektronikus változat
Intézményi repozitóriumban (DEA) tárolt változat
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3.

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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