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1.

001-es BibID:BIBFORM020469
Első szerző:Csont Tamás
Cím:Direct myocardial anti-ischaemic effect of GTN in both nitrate-tolerant and nontolerant rats : a cyclic GMP-independent activation of KATP / Tamás Csont, Zoltán Szilvássy, Ferenc Fülöp, Saviana Nedeianu, Tibor Páli, Árpád Tósaki, László Dux, Péter Ferdinandy
Dátum:1999
ISSN:0007-1188
Megjegyzések:Abstract1. We have recently demonstrated that glyceryl trinitrate (GTN) exerts a direct myocardial anti-ischaemic effect in both GTN-tolerant and nontolerant rats. Here we examined if this effect is mediated by GTN-derived nitric oxide (NO) and involves guanosine 3'5' cyclic monophosphate (cyclic GMP) and ATP-sensitive K+ channels (KATP). 2. Rats were treated with 100 mg kg-1 GTN or vehicle s.c. three times a day for 3 days to induce vascular GTN-tolerance or nontolerance. Isolated working hearts obtained from either GTN-tolerant or nontolerant rats were subjected to 10 min coronary occlusion in the presence of 10-7 M GTN or its solvent. 3. GTN improved myocardial function and reduced lactate dehydrogenase (LDH) release during coronary occlusion in both GTN-tolerant and nontolerant hearts. 4. Cardiac NO content significantly increased after GTN administration in both GTN-tolerant and nontolerant hearts as assessed by electron spin resonance. However, cardiac cyclic GMP content measured by radioimmunoassay was not changed by GTN administration. 5. When hearts from both GTN-tolerant and nontolerant rats were subjected to coronary occlusion in the presence of the KATP-blocker glibenclamide (10-7 M), the drug itself did not affect myocardial function and LDH release, however, it abolished the anti-ischaemic effect of GTN. 6. We conclude that GTN opens KATP via a cyclic GMP-independent mechanism, thereby leading to an anti-ischaemic effect in the heart in both GTN-tolerant and nontolerant rats.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Direct myocardial
anti-ischaemic effect
Direct myocardial anti-ischaemic effect
effect of GTN
GTN
cyclic activation of K(ATP)
cyclic GMP-independent activation of K(ATP)
K(ATP)
Megjelenés:British Journal of Pharmacology 128 : 7 (1999), p. 1427-1434. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Fülöp Ferenc (Szeged) Nedeianu, Saviana Páli Tibor Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Dux László Ferdinándy Péter
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2.

001-es BibID:BIBFORM052173
Első szerző:Czikora Ágnes (molekuláris biológus)
Cím:Structure-activity relationships of vanilloid receptor agonists for arteriolar TRPV1 / Á. Czikora, E. Lizanecz, P. Bakó, I. Rutkai, F. Ruzsnavszky, J. Magyar, R. Pórszász, T. Kark, A. Facskó, Z. Papp, I. Édes, A. Tóth
Dátum:2012
ISSN:0007-1188
Megjegyzések:Summary Background and purpose: The vanilloid receptor 1 (TRPV1) plays a role in the activation of sensory neurons by various painful stimuli and became a therapeutic target. However, functional TRPV1 expression was also observed in the peripheral arteries affecting microvascular diameter. Experimental approach: Sensory TRPV1 activation was measured by eye wiping tests. Arteriolar TRPV1 mediated smooth muscle specific responses (arteriolar diameter, changes in intracellular Ca2+) were determined in isolated, pressurized skeletal muscle arterioles (from the rat and wild type or TRPV1-/- mice, n = 130) or in isolated canine smooth muscle cells. Vascular pharmacology of TRPV1 agonists (potency, efficacy, kinetics of action and receptor desensitization) was determined in isolated skeletal muscle arteries of the rat. Key results: Capsaicin evoked a similar constriction as norepinephrine, which was absent in TRPV knockout mice and was competitively inhibited by a TRPV1 antagonist AMG9810. Capsaicin activation resulted in an increase in intracellular Ca2+ in the arteriolar wall as well as in isolated smooth muscle cells. Other TRPV1 agonists evoked similar vascular constrictions (MSK-195, JYL-79) or were without effect (resiniferatoxin, JYL-273), although all resulted in a sensory activation (eye wiping). Maximal dose of agonists gave different kinetics of arteriolar response. A complete desensitization (tachyphylaxis) of arteriolar TRPV1 was observed (with the exception of capsaicin). Application of the partial agonist JYL-1511 suggested that about 10% TRPV1 activation is sufficient to evoke vascular tachyphylaxis without sensory activation. Conclusions and implications: Our data suggests that arteriolar TRPV1 has different structure-activity relationship compared to sensory neuron located receptor in the rat.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
vanilloid receptor (TRPV1)
resistance artery
vascular autoregulation
Megjelenés:British Journal of Pharmacology. - 165 : 6 (2012), p. 1801-1812. -
További szerzők:Lizanecz Erzsébet (1978-) (orvos) Bakó P. Rutkai Ibolya (1985-) (molekuláris biológus) Ruzsnavszky Ferenc (1984-) (élettanász) Magyar János (1961-) (élettanász) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Kark Tamás (1981-) (orvos) Facskó Andrea (1953-) (szemész) Papp Zoltán (1965-) (kardiológus, élettanász) Édes István (1952-) (kardiológus) Tóth Attila (1971-) (biológus)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Vascularis rizikó- és stroke betegek vizsgálata
K68077
OTKA
K84300
OTKA
ETT 377/2009
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Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM013054
Első szerző:Harmati Gábor (élettanász)
Cím:Effects of β-adrenoceptor stimulation on delayed rectifier K(+) currents in canine ventricular cardiomyocytes / Harmati G., Bányász T., Bárándi L., Szentandrássy N., Horváth B., Szabó G., Szentmiklósi J., Szénási G., Nánási P., Magyar J.
Dátum:2011
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
isoproterenol
beta adrenerg
canine
cardiomyocyte
ionic current
Megjelenés:British Journal of Pharmacology. - 162 : 4 (2011), p. 890-896. -
További szerzők:Bányász Tamás (1960-) (élettanász) Bárándi László (1984-) (élettanász) Szentandrássy Norbert (1976-) (élettanász) Horváth Balázs (1981-) (élettanász) Szabó G. (orvos) Szentmiklósi József András (1948-) (farmakológus, klinikai laboratóriumi szakorvos) Szénási Gábor Nánási Péter Pál (1956-) (élettanász) Magyar János (1961-) (élettanász)
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4.

001-es BibID:BIBFORM040213
Első szerző:Helyes Zsuzsanna
Cím:Effects of the somatostatin receptor subtype 4 selective agonist J-2156 on sensory neuropeptide release and inflammatory reactions in rodents / Z. Helyes, E. Pintér, J. Németh, K. Sándor, K. Elekes, A. Szabó, G. Pozsgai, D. Keszthelyi, L. Kereskai, M. Engström, S. Wurster, J. Szolcsányi
Dátum:2006
ISSN:0007-1188
Megjegyzések:Substance P (SP) and calcitonin gene-related peptide (CGRP) released from capsaicin-sensitivesensory nerves induce local neurogenic inflammation; somatostatin exerts systemic anti-inflammatory actions presumably viasst4/sst1 receptors. This study investigates the effects of a high affinity, sst4-selective, synthetic agonist, J-2156, on sensoryneuropeptide release in vitro and inflammatory processes in vivo.Experimental approach: Electrically-induced SP, CGRP and somatostatin release from isolated rat tracheae was measuredwith radioimmunoassay. Mustard oil-induced neurogenic inflammation in rat hindpaw skin was determined by Evans blueleakage and in the mouse ear with micrometry. Dextran-, carrageenan- or bradykinin-induced non-neurogenic inflammationwas examined with plethysmometry or Evans blue, respectively. Adjuvant-induced chronic arthritis was assessed byplethysmometry and histological scoring. Granulocyte accumulation was determined with myeloperoxidase assay and IL-1bwith ELISA.Key results: J-2156 (10-2000 nM) diminished electrically-evoked neuropeptide release in a concentration-dependentmanner. EC50 for the inhibition of substance P, CGRP and somatostatin release were 11.6 nM, 14.3nM and 110.7 nM,respectively. J-2156 (1-100 mgkg-1 i.p.) significantly, but not dose-dependently, inhibited neurogenic and non-neurogenicacute inflammatory processes and adjuvant-induced chronic oedema and arthritic changes. Endotoxin-evoked myeloperoxidaseactivity and IL-1b production in the lung, but not IL-1b- or zymosan-induced leukocyte accumulation in the skin weresignificantly diminished by J-2156.Conclusions and implications: J-2156 acting on sst4 receptors inhibits neuropeptide release, vascular components of acuteinflammatory processes, endotoxin-induced granulocyte accumulation and IL-1b synthesis in the lung and synovial andinflammatory cells in chronic arthritis. Therefore it might be a promising lead for the development of novel anti-inflammatorydrugs.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:British Journal Of Pharmacology. - 149 : 4 (2006), p. 405-415. -
További szerzők:Pintér E. Németh József (1954-) (vegyész, analitikus) Sándor K. Elekes K. Pozsgai Gábor Keszthelyi Dániel Kereskai László Engström, M. Wurster, S. Szolcsányi János (Pécs)
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5.

001-es BibID:BIBFORM045973
035-os BibID:PMID:12871836
Első szerző:Pórszász Róbert (farmakológus, klinikai farmakológus)
Cím:Hepatic insulin sensitizing substance : a novel 'sensocrine' mechanism to increase insulin sensitivity in anaesthetized rats / Robert Porszasz, Gyorgyi Legvari, Tunde Pataki, Judith Szilvassy, Jozsef Nemeth, Peter Kovacs, Gyorgy Paragh, Janos Szolcsanyi, Zoltan Szilvassy
Dátum:2003
ISSN:0007-1188
Megjegyzések:We recently described the sensory nitrergic nature of the hepatic insulin sensitizing substance (HISS) mechanism linked to postprandial activation of anterior hepatic plexus fibres in rabbits. This study is designed to assess the involvement of the sensory pathways in this mechanism. 2. Selective sensory denervation of the anterior hepatic plexus (AHP) was achieved by a 3-day perineurial treatment with 2% capsaicin solution in Wistar rats (230-250 g). After 1 week, hyperinsulinaemic (100 micro U kg(-1)) euglycaemic (5.5 mmol kg(-1)) glucose clamp studies were performed to estimate insulin sensitivity. 3. The rats with regional AHP sensory denervation exhibited a significantly decreased insulin sensitivity, that is, 9.1+/-1.0 mg kg(-1) min(-1) glucose reinstalled euglycaemia vs 13.3+/-1.9 mg kg(-1) min(-1) glucose (P<0.01) in control rats. 4. Acute partial hepatic denervation by AHP cut was without effect on insulin sensitivity, whereas chronic hepatic denervation induced insulin resistance was similar to that achieved by regional AHP capsaicin treatment. 5. Intraportal administration of L-NAME (10 mg kg(-1)) decreased, whereas capsaicin (0.3 mg kg(-1) min(-1)) increased insulin sensitivity. Neither atropine (1 mg kg(-1)) nor acetylcholine (1-10 micro g mg min(-1)) produced any significant effect. In animals with preceding regional capsaicin desensitization, none of the pharmacological manoeuvres modified the resulting insulin-resistant state. 6. Cysteamine (200 mg kg(-1) s.c.) is known to cause functional somatostatin depletion-induced insulin resistance similar to that produced by either chronic partial hepatic denervation or perineurial AHP capsaicin desensitization. Intraportal capsaicin (0.3 mg kg(-1) min(-1)) was unable to modify insulin resistance achieved by cysteamine. 7. We conclude that capsaicin-sensitive sensory fibres play a crucial role in neurogenic insulin sensitization known as the HISS mechanism without involvement of anatomical reflex-mediated circuits. The results also suggest that HISS is identical to somatostatin of AHP sensory neural origin.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:British Journal of Pharmacology. - 139 : 6 (2003), p. 1171-1179. -
További szerzők:Légvári Györgyi Pataki Tünde (1971-) (farmakológus, klinikai farmakológus) Szilvássy Judit (1960-2022) (fül- orr- gégész) Németh József (Pécs) Kovács Péter (1939-) (farmakológus) Paragh György (1953-) (belgyógyász) Szolcsányi János (Pécs) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM099194
035-os BibID:(WOS)000751415800001 (Scopus)85124483518
Első szerző:Priksz Dániel (farmakológus)
Cím:Nicotinic-acid derivative BGP-15 improves diastolic function in a rabbit model of atherosclerotic cardiomyopathy / Priksz Daniel, Lampe Nora, Kovacs Arpad, Herwig Melissa, Bombicz Mariann, Varga Balazs, Wilisicz Tician, Szilvassy Judit, Posa Aniko, Kiss Rita, Gesztelyi Rudolf, Raduly Arnold, Szekeres Reka, Sieme Marcel, Papp Zoltan, Toth Attila, Hamdani Nazha, Szilvassy Zoltan, Juhasz Bela
Dátum:2022
ISSN:0007-1188
Megjegyzések:Background and purpose: Small molecule BGP-15 has been reported to alleviate signs of heart failure and improve muscle function in murine models. Here, we investigated the acute and chronic effects of BGP-15 in a rabbit model of atherosclerotic cardiomyopathy. Experimental approach: Rabbits were maintained on standard chow (Control) or atherogenic diet (HC) for 16 weeks. BGP-15 was administered intravenously (once) or orally (for 16 weeks), to assess acute and chronic effects. Cardiac function was evaluated by echocardiography, endothelium-dependent vasorelaxation was assessed, and key molecules of the protein kinase G (PKG) axis were examined by ELISA and Western blot. Passive force generation was investigated in skinned cardiomyocytes. Key results: Both acute and chronic BGP-15 treatment improved the diastolic performance of the diseased heart, however, vasorelaxation and serum lipid markers were unaffected. Myocardial cGMP levels were elevated in the BGP-15-treated group, along with preserved PKG activity and increased phospholamban Ser16-phosphorylation. PDE5 expression decreased in the BGP-15-treated group, and the substance inhibited PDE1 enzyme. Cardiomyocyte passive tension reduced in BGP-15-treated rabbits, the ratio of titin N2BA/N2B isoforms increased, and PKG-dependent N2B-titin phosphorylation elevated in the BGP-15-treated group. Conclusions and implications: Here we report that BGP-15-treatment improves diastolic function, reduces cardiomyocyte stiffness, and restores titin compliance in a rabbit model of atherosclerotic cardiomyopathy by increasing the activity of the cGMP-PKG axis. As BGP-15 is proven to be safe, it may have clinical value in the treatment of diastolic dysfunction.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
BGP-15
diastolic dysfunction
hypercholesterolemia
protein kinase G
titin
Megjelenés:British Journal Of Pharmacology. - 179 : 10 (2022), p. 2240-2258. -
További szerzők:Lampé Nóra Kovács Árpád (1986-) (kardiológus) Herwig, Melissa Bombicz Mariann (1987-) (gyógyszerész) Varga Balázs (1984-) (kísérletes farmakológus) Wilisicz, Tician Szilvássy Judit (1960-2022) (fül- orr- gégész) Pósa Anikó Kiss Rita (1974-) (laboratóriumi diagnosztika szakorvos) Gesztelyi Rudolf (1969-) (kísérletes farmakológus) Ráduly Arnold Péter (1993-) Szekeres Réka (1995-) (orvos) Sieme, Marcel Papp Zoltán (1965-) (kardiológus, élettanász) Tóth Attila (1971-) (biológus) Hamdani, Nazha Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Juhász Béla (1978-) (kísérletes farmakológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00043
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TKP2020-IKA-04
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