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001-es BibID:	BIBFORM018437
Első szerző:	Bagi Zsolt (orvos)
Cím:	Preserved coronary arteriolar dilatation in patients with type 2 diabetes mellitus: Implications for reactive oxygen species / Bagi Zsolt, Feher Attila, Beleznai Timea
Dátum:	2009
ISSN:	1734-1140
Megjegyzések:	Type 2 diabetes mellitus is associated with clustering of cardiovascular risk factors that may greatly increase individuals' risk of developing coronary artery disease. Type 2 diabetes is believed to impair coronary function. However, its impact on the vasomotor function of coronary resistance vessels in humans is still debated. Reduced, preserved or even augmented dilations of coronary arterioles have been reported in subjects with type 2 diabetes. Interestingly, recent studies have suggested that reactive oxygen species (ROS), particularly hydrogen peroxide, may compensate for the loss of the vasodilatory function of coronary microvessels during disease development. Recent interventional clinical trials have yielded largely negative results, and there has even been some suggestion of harm caused by attempts to reduce ROS. Thus, it is possible that interference with ROS-related signaling might paradoxically temper the function of coronary microvessels, predisposing patients to myocardial ischemia. In this review, we aim to highlight current findings supporting a potential role for ROS in preserving coronary arteriolar dilation in type 2 diabetes mellitus.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban diabetes coronary arteriole H2O2 antioxidant
Megjelenés:	Pharmacological Reports. - 61 : 1 (2009), p. 99-104. -
További szerzők:	Fehér Attila (1982-) (orvos) Beleznai Tímea (1981-) (orvos)
Pályázati támogatás:	F-048837 OTKA
Internet cím:	Szerző által megadott URL Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM029129
Első szerző:	Beleznai Tímea (orvos)
Cím:	Arginase 1 contributes to diminished coronary arteriolar dilation in patients with diabetes / Beleznai T., Feher A., Spielvogel D., Lansman S. L., Bagi Z.
Dátum:	2011
ISSN:	0363-6135
Megjegyzések:	Arginase 1, via competing with nitric oxide (NO) synthase for the substrate L-arginine, may interfere with NO-mediated vascular responses. We tested the hypothesis that arginase 1 contributes to coronary vasomotor dysfunction in patients with diabetes mellitus (DM). Coronary arterioles were dissected from the right atrial appendages of 41 consecutive patients with or without DM (the 2 groups suffered from similar comorbidities), and agonist-induced changes in diameter were measured with videomicroscopy. We found that the endothelium-dependent agonist ACh elicited a diminished vasodilation and caused constriction to the highest ACh concentration (0.1 mikroM) with a similar magnitude in patients with (18 ± 8%) and without (17 ± 9%) DM. Responses to ACh were not significantly affected by the inhibition of NO synthesis with N(G)-nitro-L-arginine methyl ester in either group. The NO donor sodium nitroprusside-dependent dilations were not different in patients with or without DM. Interestingly, we found that the presence of N(G)-hydroxy-L-arginine (10 mikroM), a selective inhibitor of arginase or application of L-arginine (3 mM), restored ACh-induced coronary dilations only in patients with DM (to 47 ± 6% and to 40 ± 19%, respectively) but not in subjects without DM. Correspondingly, the protein expression of arginase 1 was increased in coronary arterioles of patients with DM compared with subjects without diabetes. Moreover, using immunocytochemistry, we detected an abundant immunostaining of arginase 1 in coronary endothelial cells of patients with DM, which was colocalized with NO synthase. Collectively, we provided evidence for a distinct upregulation of arginase 1 in coronary arterioles of patients with DM, which contributes to a reduced NO production and consequently diminished vasodilation.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	American Journal Of Physiology-Heart And Circulatory Physiology. - 300 : 3 (2011), p. H777-H783. -
További szerzők:	Fehér Attila (1982-) (orvos) Spielvogel, David Lansman, Steven L. Bagi Zsolt (1974-) (orvos)
Pályázati támogatás:	RE/08/004 Egyéb
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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001-es BibID:	BIBFORM029128
Első szerző:	Beleznai Tímea (orvos)
Cím:	Activation of hexosamine pathway impairs nitric oxide (NO)-dependent arteriolar dilations by increased protein O-GlcNAcylation / Beleznai Timea, Bagi Zsolt
Dátum:	2012
ISSN:	1537-1891
Megjegyzések:	We hypothesized that under high glucose conditions, activation of the hexosamine pathway leads to impaired nitric oxide (NO)-dependent arteriolar dilation. Skeletal muscle arterioles (diameter: ~160mikrom) isolated from male Wistar rats were exposed to normal glucose (NG, 5.5mmol/L) or high glucose concentrations (HG, 30mmol/L, for 2h) and agonist-induced diameter changes were measured with videomicroscopy. Western blots were performed to identify the vascular levels of protein O-linked-N-acetyl-glucosamine (O-GlcNAc) and phosphorylated endothelial NO synthase (eNOS). In arterioles exposed to HG, dilations to histamine were abolished compared to those exposed to NG (max: -6±6% and 69±9%, respectively), while acetylcholine-induced responses were not affected. Inhibition of NO synthesis with N(G)-nitro-l-arginine methyl ester (L-NAME) reduced histamine-induced dilations in NG arterioles, but it had no effect on microvessels exposed to HG. Dilations to the NO donor, sodium nitroprusside and constrictions to norepinephrine and serotonin were similar in the two groups. In the presence of the inhibitor of hexosamine pathway, azaserine, histamine-induced dilations were significantly augmented in arterioles exposed to HG (max: 67±2%). Moreover, exposure of vessels to glucosamine (5mmol/L, for 2h) resulted in reduced histamine-induced arteriolar dilations (max: 26±3%). The level of protein O-GlcNAcylation was increased, whereas the P-eNOS (Ser-1177) was decreased in HG exposed vessels. These findings indicate that a high concentration of glucose may lead to glucosamine formation, which impairs histamine-induced, NO-mediated arteriolar dilations. We propose that interfering with the hexosamine pathway may prevent microvascular complications in diabetes.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Vascular Pharmacology. - 56 : 3-4 (2012), p. 115-121. -
További szerzők:	Bagi Zsolt (1974-) (orvos)
Pályázati támogatás:	RE/08/004 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM018438
Első szerző:	Fehér Attila (orvos)
Cím:	Caveolin-1 limits the contribution of BK(Ca) channel to EDHF-mediated arteriolar dilation: implications in diet-induced obesity / Feher, A., Rutkai, I., Beleznai, T., Ungvari, Z., Csiszar, A., Edes, I., Bagi, Z.
Dátum:	2010
ISSN:	0008-6363
Megjegyzések:	Caveolin-1 (Cav-1) interacts with large conductance Ca(2+)-activated potassium channels (BKCa) and likely exerts a negative regulatory effect on the channel activity. We investigated the role of Cav-1 in modulating BK(Ca) channel-mediated, endothelium-derived hyperpolarizing factor (EDHF)-dependent arteriolar dilation in normal condition and in an experimental model of obesity. METHODS AND RESULTS: In isolated, pressurized (80 mmHg) gracilis muscle arterioles (approximately 100 microm) of Cav-1 knockout mice, acetylcholine (ACh)-induced, EDHF-mediated dilations were enhanced and were significantly reduced by the BK(Ca) channel inhibitor, iberiotoxin (IBTX), whereas IBTX had no effect on EDHF-mediated dilations in the wild-type mice. Dilations to the selective BK(Ca) channel opener, NS-1619 were augmented in the Cav-1 knockout mice. In high-fat diet-treated, obese rats ACh-induced coronary arteriolar dilations were preserved, whereas IBTX-sensitive, ACh-induced and also NS-1619-evoked vasodilations were augmented when compared with lean animals. In coronary arterioles of obese rats a reduced protein expression of Cav-1 was detected by western immunoblotting and immunohistochemistry. Moreover, in coronary arterioles of lean rats, disruption of caveolae with methyl-beta-cyclodextrin augmented IBTX-sensitive, ACh-induced, and also NS-1619-evoked dilations. CONCLUSION: Thus, under normal conditions, Cav-1 limits the contribution of the BK(Ca) channel to EDHF-mediated arteriolar dilation. In obesity, a reduced expression of Cav-1 leads to greater contribution of the BK(Ca) channel to EDHF-mediated response, which seems essential for maintained coronary dilation.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Coronary Microcirculation EDHF MaxiK channel Caveolae
Megjelenés:	Cardiovascular Research. - 87 : 4 (2010), p. 732-739. -
További szerzők:	Rutkai Ibolya (1985-) (molekuláris biológus) Beleznai Tímea (1981-) (orvos) Ungvári Zoltán Csiszár Anna Édes István (1952-) (kardiológus) Bagi Zsolt (1974-) (orvos)
Pályázati támogatás:	0735540T Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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