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1.

001-es BibID:BIBFORM058137
Első szerző:Bagi Zsolt (orvos)
Cím:Type 2 diabetic mice have increased arteriolar tone and blood pressure : enhanced release of COX-2-derived constrictor prostaglandins / Zsolt Bagi, Nora Erdei, Attila Toth, Wei Li, Thomas H. Hintze, Akos Koller, Gabor Kaley
Dátum:2005
ISSN:1079-5642
Megjegyzések:OBJECTIVE: Type 2 diabetes mellitus (T2-DM) is frequently associated with vascular dysfunction and elevated blood pressure, yet the underlying mechanisms are not completely understood. We hypothesized that in T2-DM, the regulation of peripheral vascular resistance is altered because of changes in local vasomotor mechanisms. METHODS AND RESULTS: In mice with T2-DM (C57BL/KsJ-(db-)/db-), systolic and mean arterial pressures measured by the tail cuff method were significantly elevated compared with those of control (db+/db-) animals (db/db, 146+/-5 and 106+/-2 mm Hg versus control, 133+/-4 and 98+/-4 mm Hg, respectively; P<0.05). Total peripheral resistance, calculated from cardiac output values (measured by echocardiography) and mean arterial pressure were significantly elevated in db/db mice (db/db, 25+/-6 versus control, 15+/-1 mm Hg[middot]mL(-1)[middot]min(-1)). In isolated, pressurized gracilis muscle arterioles (diameter approximately 80 microm) from db/db mice, stepwise increases in intraluminal pressure (from 20 to 120 mm Hg) elicited a greater reduction in diameter than in control vessels at each pressure step (at 80 mm Hg, db/db, 66+/-4% versus control, 79+/-3%). The passive diameters of arterioles (obtained in Ca2+-free solution) and the calculated myogenic index were not significantly different in the 2 groups. The presence of the prostaglandin H2/thromboxane A2 receptor antagonist SQ29548 did not affect arteriolar diameters of control mice but reduced the enhanced arteriolar tone of db/db mice back to control levels (at 80 mm Hg, 80+/-4%). The inhibitor of cyclooxygenase-1 (COX-1), SC-560, did not affect the basal tone of arterioles, whereas NS-398, an inhibitor of COX-2, caused a significant shift in the arteriolar pressure-diameter curve of vessels from db/db mice (at 80 mm Hg, 76+/-3%) but not in those of control mice. Also, in aortas of db/db mice, expression of COX-2 was enhanced compared with controls. CONCLUSIONS: Collectively, these findings suggest that in mice with T2-DM, the basal tone of skeletal muscle arterioles is increased because of an enhanced COX-2-dependent production of constrictor prostaglandins. These alterations in microvascular prostaglandin synthesis may contribute to the increase in peripheral resistance and blood pressure in T2-DM.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Arteriosclerosis Thrombosis and Vascular Biology. - 25 : 8 (2005), p. 1610-1616. -
További szerzők:Erdei Nóra (1979-) (orvos) Tóth Attila (1971-) (biológus) Li, Wei (1987-) (kutató) Hintze, Thomas H. Koller Ákos Kaley Gábor
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2.

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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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:BIBFORM017934
Első szerző:Molnár Andrea (kardiológus)
Cím:Activation of the Poly(ADP-Ribose) Polymerase Pathway in Human Heart Failure / Andrea Molnár, Attila Tóth, Zsolt Bagi, Zoltán Papp, István Édes, Miklós Vaszily, Zoltán Galajda, Julius Gy. Papp, András Varró, Viktória Szüts, Zsombor Lacza, Domokos Gerö, Csaba Szabó
Dátum:2006
ISSN:1076-1551
Megjegyzések:Poly(ADP-ribose) polymerase (PARP) activation has been implicated in the pathogenesis of acute and chronic myocardial dysfunction and heart failure. The goal of the present study was to investigate PARP activation in human heart failure, and to correlate PARP activation with various indices of apoptosis and oxidative and nitrosative stress in healthy (donor) and failing (NYHA class III-IV) human heart tissue samples. Higher levels of oxidized protein end-products were found in failing hearts compared with donor heart samples. On the other hand, no differences in tyrosine nitration (a marker of peroxynitrite generation) were detected. Activation of PARP was demonstrated in the failing hearts by an increased abundance of poly-ADP ribosylated proteins. Immunohistochemical analysis revealed that PARP activation was localized to the nucleus of the cardiomyocytes from the failing hearts. The expression of full-length PARP-1 was not significantly different in donor and failing hearts. The expression of caspase-9, in contrast, was significantly higher in the failing than in the donor hearts. Immunohistochemical analysis was used to detect the activation of mitochondrial apoptotic pathways. We found no significant translocation of apoptosis-inducing factor (AIF) into the nucleus. Overall, the current data provide evidence of oxidative stress and PARP activation in human heart failure. Interventional studies with antioxidants or PARP inhibitors are required to define the specific roles of these factors in the pathogenesis of human heart failure
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Molecular Medicine. - 12 : 7-8 (2006), p. 143-152. -
További szerzők:Tóth Attila (1971-) (biológus) Bagi Zsolt (1974-) (orvos) Papp Zoltán (1965-) (kardiológus, élettanász) Édes István (1952-) (kardiológus) Vaszily Miklós (1949-) (szívsebész) Galajda Zoltán (1962-) (szívsebész, érsebész) Papp Gy. Julius (Szeged) Varró András (1954-) (farmakológus, klinikai farmakológus) Szűts Viktória (farmakológus Szeged) Lacza Zsombor Gerö Domokos (Budapest) Szabó Csaba (1967-) (orvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM040608
Első szerző:Tóth Attila (biológus)
Cím:Expression and distribution of vanilloid receptor 1 (TRPV1) in the adult rat brain / Toth, A., Boczan, J., Kedei, N., Lizanecz, E., Bagi, Z., Papp, Z., Edes, I., Csiba, L., Blumberg, P. M.
Dátum:2005
ISSN:0169-328X
Megjegyzések:The vanilloid receptor (TRPV1 or VR1) is a molecular integrator of various painful stimuli, including capsaicin, acid, and high temperature. It can also be activated by endogenous ligands, like the cannabinoid 1 receptor (CB1) agonist anandamide. TRPV1 is well characterized at the terminals of sensory nerves involved in the pain pathway. There is also evidence that TRPV1 is expressed in the brain but little is known about its function. Here, using commercially available specific antibodies to investigate the localization of TRPV1 in the brain of the rat, we report that TRPV1 was expressed in hippocampus, cortex, cerebellum, olfactory bulb, mesencephalon and hindbrain. Immunohistochemical analyses showed high expression in the cell bodies and dendrites of neurons in the hippocampus and in the cortex. To address the question of subcellular localization, immunoelectronmicroscopy was used. TRPV1-like staining was detected in the synapses (mostly, but not exclusively in post-synaptic dendritic spines), on the end feet of astrocytes and in pericytes. In summary, TRPV1 expression shows wide distribution in the brain of the rat, being found in astrocytes and pericytes as well as in neurons. Its localization is consistent with multiple functions within the central nervous system, including the regulation of brain vasculature.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Molecular Brain Research. - 135 : 1-2 (2005), p. 162-168. -
További szerzők:Boczán Judit (1972-) (neurológus) Kedei Noémi Lizanecz Erzsébet (1978-) (orvos) Bagi Zsolt (1974-) (orvos) Papp Zoltán (1965-) (kardiológus, élettanász) Édes István (1952-) (kardiológus) Csiba László (1952-) (neurológus, pszichiáter) Blumberg, Peter M.
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Intézményi repozitóriumban (DEA) tárolt változat
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