CCL

Összesen 8 találat.
#/oldal:
Részletezés:
Rendezés:

1.

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
Borító:

2.

001-es BibID:BIBFORM018442
Első szerző:Bagi Zsolt (orvos)
Cím:Microvascular responsiveness in obesity : implications for therapeutic intervention / Zsolt Bagi, Attila Feher, James Cassuto
Dátum:2012
ISSN:0007-1188
Megjegyzések:Obesity has detrimental effects on the microcirculation. Functional changes in microvascular responsiveness may increase the risk of developing cardiovascular complications in obese patients. Emerging evidence indicates that selective therapeutic targeting of the microvessels may prevent life-threatening obesity-related vascular complications, such as ischemic heart disease, heart failure and hypertension. It is also plausible that alterations in adipose tissue microcirculation contribute to the development of obesity. Therefore, targeting adipose tissue arterioles could represent a novel approach to reducing obesity. This review aims to examine recent studies that have been focused on vasomotor dysfunction of resistance arteries in obese humans and animal models of obesity. Particularly, findings in coronary resistance arteries are contrasted to those obtained in other vascular beds. We provide examples of therapeutic attempts, such as use of statins, angiotensin converting enzyme inhibitors and insulin sensitizers to prevent obesity-related microvascular complications. We further identify some of the important challenges and opportunities going forward.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
obesity
microcirculation
arteriole
coronary
type 2 diabetes mellitus
Megjelenés:British Journal Of Pharmacology. - 165 : 3 (2012), p. 544-560. -
További szerzők:Fehér Attila (1982-) (orvos) Cassuto, James
Pályázati támogatás:R01 HL104126
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

001-es BibID:BIBFORM018441
Első szerző:Bagi Zsolt (orvos)
Cím:Increased availability of angiotensin AT1 receptors leads to sustained arterial constriction to angiotensin II in diabetes - role for Rho-kinase activation / Zsolt Bagi, Attila Feher, James Cassuto, Komala Akula, Nazar Labinskyy, Gabor Kaley, Akos Koller
Dátum:2011
ISSN:0007-1188
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
diabetes mellitus
hyperglycaemia
arteriolar constriction
AT1 receptor
Rho-kinase
Megjelenés:British Journal Of Pharmacology. - 163 : 5 (2011), p. 1059-1068. -
További szerzők:Fehér Attila (1982-) (orvos) Cassuto, James Akula, Komala Labinskyy, Nazar Kaley Gábor Koller Ákos
Pályázati támogatás:K71591
OTKA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

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
Borító:

5.

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
Borító:

6.

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
DOI
Borító:

7.

001-es BibID:BIBFORM018436
Első szerző:Rutkai Ibolya (molekuláris biológus)
Cím:Activation of prostaglandin E2 EP1 receptor increases arteriolar tone and blood pressure in mice with type 2 diabetes / Rutkai, I., Feher, A., Erdei, N., Henrion, D., Papp, Z., Edes, I., Koller, A., Kaley, G., Bagi, Z.
Dátum:2009
ISSN:0008-6363
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
diabetes
hypertension
arteriole
prostanoid
EP receptor
Megjelenés:Cardiovascular Research. - 83 : 1 (2009), p. 148-154. -
További szerzők:Fehér Attila (1982-) (orvos) Erdei Nóra (1979-) (orvos) Henrion, Daniel Papp Zoltán (1965-) (kardiológus, élettanász) Édes István (1952-) (kardiológus) Koller Ákos Kaley Gábor Bagi Zsolt (1974-) (orvos)
Pályázati támogatás:449/2006
OTKA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

8.

001-es BibID:BIBFORM018439
Első szerző:Ungvári Zoltán
Cím:Resveratrol confers endothelial protection via activation of the antioxidant transcription factor Nrf2 / Ungvari, Z., Bagi, Z., Feher, A., Recchia, F. A., Sonntag, W. E., Pearson, K., de Cabo, R., Csiszar, A.
Dátum:2010
ISSN:0363-6135
Megjegyzések:Epidemiological studies suggest that Mediterranean diets rich in resveratrol are associated with reduced risk of coronary artery disease. Resveratrol was also shown to confer vasoprotection in animal models of type 2 diabetes and aging. However, the mechanisms by which resveratrol exerts its antioxidative vasculoprotective effects are not completely understood. Using a nuclear factor-E(2)-related factor-2 (Nrf2)/antioxidant response element-driven luciferase reporter gene assay, we found that in cultured coronary arterial endothelial cells, resveratrol, in a dose-dependent manner, significantly increases transcriptional activity of Nrf2. Accordingly, resveratrol significantly upregulates the expression of the Nrf2 target genes NAD(P)H:quinone oxidoreductase 1, gamma-glutamylcysteine synthetase, and heme oxygenase-1. Resveratrol treatment also significantly attenuated high glucose (30 mM)-induced mitochondrial and cellular oxidative stress (assessed by flow cytometry using MitoSox and dihydroethidine staining). The aforementioned effects of resveratrol were significantly attenuated by the small interfering RNA downregulation of Nrf2 or the overexpression of Kelch-like erythroid cell-derived protein 1, which inactivates Nrf2. To test the effects of resveratrol in vivo, we used mice fed a high-fat diet (HFD), which exhibit increased vascular oxidative stress associated with an impaired endothelial function. In HFD-fed Nrf2(+/+) mice, resveratrol treatment attenuates oxidative stress (assessed by the Amplex red assay), improves acetylcholine-induced vasodilation, and inhibits apoptosis (assessed by measuring caspase-3 activity and DNA fragmentation) in branches of the femoral artery. In contrast, the aforementioned endothelial protective effects of resveratrol were diminished in HFD-fed Nrf2(-/-) mice. Taken together, our results indicate that resveratrol both in vitro and in vivo confers endothelial protective effects which are mediated by the activation of Nrf2.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
endothelial cell
gracilis
resveratrol
nuclear factor-E2-related factor- 2
Megjelenés:American Journal of Physiology. Heart and Circulatory Physiology. - 299 : 1 (2010), p. H18-H24. -
További szerzők:Bagi Zsolt (1974-) (orvos) Fehér Attila (1982-) (orvos) Recchia, Fabio A. Sonntag, William E. Pearson, Kevin de Cabo, Rafael Csiszár Anna
Pályázati támogatás:HL-077256
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1 
Corvina könyvtári katalógus v8.2.27 © 2023 Monguz kft. Minden jog fenntartva.