CCL

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1.

001-es BibID:BIBFORM020103
Első szerző:Erdei Nóra (orvos)
Cím:High-fat diet-induced reduction in nitric oxide-dependent arteriolar dilation in rats: role of xanthine oxidase-derived superoxide anion / Nóra Erdei, Attila Tóth, Enikő T. Pásztor, Zoltán Papp, István Édes, Akos Koller, Zsolt Bagi
Dátum:2006
ISSN:0363-6135
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal Of Physiology-Heart And Circulatory Physiology. - 291 : 5 (2006), p. H2107-H2115. -
További szerzők:Tóth Attila (1971-) (biológus) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Papp Zoltán (1965-) (kardiológus, élettanász) Édes István (1952-) (kardiológus) Koller Ákos Bagi Zsolt (1974-) (orvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM005634
Első szerző:Jebelovszki Éva
Cím:High-fat diet-induced obesity leads to increased NO sensitivity of rat coronary arterioles : role of soluble guanylate cyclase activation / Jebelovszki, E., Kiraly, C., Erdei, N., Feher, A., Pasztor, T. E., Rutkai, I., Forster, T., Edes, I., Koller, A., Bagi, Z.
Dátum:2008
ISSN:0363-6135 (Print)
Megjegyzések:The impact of obesity on nitric oxide (NO)-mediated coronary microvascular responses is poorly understood. Thus NO-mediated vasomotor responses were investigated in pressurized coronary arterioles ( approximately 100 microm) isolated from lean (on normal diet) and obese (fed with 60% of saturated fat) rats. We found that dilations to acetylcholine (ACh) were not significantly different in obese and lean rats (lean, 83 +/- 4%; and obese, 85 +/- 3% at 1 microM), yet the inhibition of NO synthesis with N(omega)-nitro-l-arginine methyl ester reduced ACh-induced dilations only in vessels of lean controls. The presence of the soluble guanylate cyclase (sGC) inhibitor oxadiazolo-quinoxaline (ODQ) elicited a similar reduction in ACh-induced dilations in the two groups of vessels (lean, 60 +/- 11%; and obese, 57 +/- 3%). Dilations to NO donors, sodium nitroprusside (SNP), and diethylenetriamine (DETA)-NONOate were enhanced in coronary arterioles of obese compared with lean control rats (lean, 63 +/- 6% and 51 +/- 5%; and obese, 78 +/- 5% and 70 +/- 5%, respectively, at 1 microM), whereas dilations to 8-bromo-cGMP were not different in the two groups. In the presence of ODQ, both SNP and DETA-NONOate-induced dilations were reduced to a similar level in lean and obese rats. Moreover, SNP-stimulated cGMP immunoreactivity in coronary arterioles and also cGMP levels in carotid arteries were enhanced in obese rats, whereas the protein expression of endothelial NOS and the sGC beta1-subunit were not different in the two groups. Collectively, these findings suggest that in coronary arterioles of obese rats, the increased activity of sGC leads to an enhanced sensitivity to NO, which may contribute to the maintenance of NO-mediated dilations and coronary perfusion in obesity.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Acetylcholine
Adaptation, Physiological
Animals
Arterioles
Blotting, Western
Coronary Vessels
Cyclic GMP
Dietary Fats
Disease Models, Animal
Dose-Response Relationship, Drug
Enzyme Activation
Enzyme Inhibitors
Enzyme-Linked Immunosorbent Assay
Guanylate Cyclase
Immunohistochemistry
Male
NG-Nitroarginine Methyl Ester
Nitric Oxide
Nitric Oxide Donors
Nitric Oxide Synthase Type II
Nitroprusside
Nitroso Compounds
Obesity
Rats
Rats, Wistar
Receptors, Cytoplasmic and Nuclear
Vasodilation
Vasodilator Agents
Megjelenés:American Journal of Physiology. Heart and Circulatory Physiology. - 294 : 6 (2008), p. H2558-H2564. -
További szerzők:Király Csaba Erdei Nóra (1979-) (orvos) Fehér Attila (1982-) (orvos) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Rutkai Ibolya (1985-) (molekuláris biológus) Forster Tamás Édes István (1952-) (kardiológus) Koller Ákos Bagi Zsolt (1974-) (orvos)
Internet cím:elektronikus változat
elektronikus változat
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3.

001-es BibID:BIBFORM003870
Első szerző:Kark Tamás (orvos)
Cím:Tissue-specific regulation of microvascular diameter : opposite functional roles of neuronal and smooth muscle located vanilloid receptor-1 / Tamás Kark, Zsolt Bagi, Erzsébet Lizanecz, Enikő T. Pásztor, Nóra Erdei, Ágnes Czikora, Zoltán Papp, István Édes, Róbert Pórszász, Attila Tóth
Dátum:2008
Megjegyzések:The transient receptor potential type V1 channel (vanilloid receptor 1, TRPV1) is a Ca2+ -permeable nonspecific cation channel activated by various painful stimuli including ischemia. We hypothesized that TRPV1 is expressed in the arterioles and is involved in the regulation of microvascular tone. We found that TRPV1 stimulation by capsaicin (intra-arterial administration) of the isolated, perfused right hind limb of the rat increased vascular resistance (by 98 ± 21 mm Hg at 10 gamma g) in association with decreased skeletal muscle perfusion and elevation of skin perfusion (detected by dual-channel laser Doppler flowmetry). Denervation of the hind limb did not affect capsaicin-evoked changes in vascular resistance and tissue perfusion in the hind limb but reduced the elevation of perfusion in the skin. In isolated, pressurized skeletal (musculus gracilis) muscle arterioles (diameter, 147 ± 35 gamma m), capsaicin had biphasic effects: at lowe concentrations, capsaicin (up to 10 nM) evoked dilations (maximum, 32 ± 13%), whereas higher concentrations (0.1-1 gamma M) elicited substantial constrictions (maximum, 66 ± 7%). Endothelium removal or inhibition of nitric-oxide synthase abolished capsaicin-induced dilations but did not affect arteriolar constriction. Expression of TRPV1 was detected by reverse transcriptase-polymerase chain reaction in the aorta and in cultured rat aortic vascular smooth muscle cells (A7r5). Immunohistochemistry revealed expression primarily in the smooth muscle layers of the gracilis arteriole. These data demonstrate the functional expression of TRPV1 in vascular smooth muscle cells mediating vasoconstriction of the resistance arteries. Because of the dual effects of TRPV1 stimulation on the arteriolar diameter (dilation in skin, constriction in skeletal muscle), we propose that TRPV1 ligands represent drug candidates for tissue-specific modulation of blood distribution.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
TRPV1
CGRP
calcitonin gene-related peptide
SP
Megjelenés:Molecular Pharmacology. - 73 : 5 (2008), p. 1405-1412. -
További szerzők:Bagi Zsolt (1974-) (orvos) Lizanecz Erzsébet (1978-) (orvos) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Erdei Nóra (1979-) (orvos) Czikora Ágnes (1982-) (molekuláris biológus) Papp Zoltán (1965-) (kardiológus, élettanász) Édes István (1952-) (kardiológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Tóth Attila (1971-) (biológus)
Internet cím:elektronikus változat
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4.

001-es BibID:BIBFORM020104
Első szerző:Lizanecz Erzsébet (orvos)
Cím:Phosphorylation-Dependent Desensitization by Anandamide of Vanilloid Receptor-1 (TRPV1) Function in Rat Skeletal Muscle Arterioles and in Chinese Hamster Ovary Cells Expressing TRPV1 / Erzsébet Lizanecz, Zsolt Bagi, Enikő T. Pásztor, Zoltán Papp, István Édes, Noémi Kedei, Peter M. Blumberg, Attila Tóth
Dátum:2006
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Molecular Pharmacology. - 69 : 3 (2006), p. 1015-1023. -
További szerzők:Bagi Zsolt (1974-) (orvos) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Papp Zoltán (1965-) (kardiológus, élettanász) Édes István (1952-) (kardiológus) Kedei Noémi Blumberg, Peter M. Tóth Attila (1971-) (biológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM018115
Első szerző:Szerafin Tamás (szívsebész, mellkassebész)
Cím:Increased cyclooxygenase-2 expression and prostaglandin-mediated dilation in coronary arterioles of patients with diabetes mellitus / Szerafin T., Erdei N., Fülöp T., Pasztor T. E., Edes I., Koller A., Bagi Z.
Dátum:2006
ISSN:0009-7330
Megjegyzések:Based on findings of experimental models of diabetes mellitus (DM) showing increased expression of vascular cyclooxygenase-2 (COX-2), we hypothesized that in patients with DM changes in COX-2-dependent prostaglandin synthesis affect vasomotor responses of coronary arterioles. Arterioles were dissected from the right atrial appendages obtained at the time of cardiac surgery of patient with DM(+) or without documented diabetes DM(-). Isolated arterioles (89+/-15 microm in diameter) were cannulated and pressurized (at 80 mm Hg), and changes in diameter were measured with video microscopy. After spontaneous tone developed [DM(-): 32+/-7%; DM(+): 37+/-5%; P=NS], arteriolar responses to bradykinin were investigated. Dilations to bradykinin (0.1 nmol/L to 1 micromol/L) were significantly (P<0.05) greater in DM(+) than DM(-) patients (10 nmol/L: 77+/-10% versus 38+/-14%). In both groups, dilations were similar to the NO-donor, sodium nitroprusside. In arterioles of DM(+), but not those of DM(-), patients' bradykinin-induced dilations were reduced by the nonselective COX inhibitor indomethacin or by the selective COX-2 inhibitor NS-398 (DM(+) at 10 nmol/L: to 20+/-4% and 29+/-7%, respectively). Correspondingly, a marked COX-2 immunostaining was detected in coronary arterioles of DM(+), but not in those of DM(-) patients. We conclude that in coronary arterioles of diabetic patients bradykinin induces enhanced COX-2-derived prostaglandin-mediated dilation. These findings are the first to show that in humans diabetes mellitus increases COX-2 expression and dilator prostaglandin synthesis in coronary arterioles, which may serve to increase dilator capacity and maintain adequate perfusion of cardiac tissues.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Circulation Research. - 99 : 5 (2006), p. e12-e17. -
További szerzők:Erdei Nóra (1979-) (orvos) Fülöp Tibor (1957-) (kardiológus) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Édes István (1952-) (kardiológus) Koller Ákos Bagi Zsolt (1974-) (orvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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