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1.

001-es BibID:BIBFORM009063
Első szerző:Alvarez, Julio
Cím:ATP/UTP activate cation-permeable channels with TRPC3/7 properties in rat cardiomyocytes / Alvarez, J., Coulombe, A., Cazorla, O., Ugur, M., Rauzier, J. M., Magyar, J., Mathieu, E. L., Boulay, G., Souto, R., Bideaux, P., Salazar, G., Rassendren, F., Lacampagne, A., Fauconnier, J., Vassort, G.
Dátum:2008
ISSN:0363-6135 (Print)
Megjegyzések:Extracellular purines and pyrimidines have major effects on cardiac rhythm and contraction. ATP/UTP are released during various physiopathological conditions, such as ischemia, and despite degradation by ectonucleotidases, their interstitial concentrations can markedly increase, a fact that is clearly associated with arrhythmia. In the present whole cell patch-clamp analysis on ventricular cardiomyocytes isolated from various mammalian species, ATP and UTP elicited a sustained, nonselective cationic current, I(ATP). UDP was ineffective, whereas 2'(3')-O-(4-benzoylbenzoyl)-ATP was active, suggesting that P2Y(2) receptors are involved. I(ATP) resulted from the binding of ATP(4-) to P2Y(2) purinoceptors. I(ATP) was maintained after ATP removal in the presence of guanosine 5'-[gamma-thio]triphosphate and was inhibited by U-73122, a PLC inhibitor. Single-channel openings are rather infrequent under basal conditions. ATP markedly increased opening probability, an effect prevented by U-73122. Two main conductance levels of 14 and 23 pS were easily distinguished. Similarly, in fura-2-loaded cardiomyocytes, Mn(2+) quenching and Ba(2+) influx were significant only in the presence of ATP or UTP. Adult rat ventricular cardiomyocytes expressed transient receptor potential channel TRPC1, -3, -4, and -7 mRNA and the TRPC3 and TRPC7 proteins that coimmunoprecipitated. Finally, the anti-TRPC3 antibody added to the patch pipette solution inhibited I(ATP). In conclusion, activation of P2Y(2) receptors, via a G protein and stimulation of PLCbeta, induces the opening of heteromeric TRPC3/7 channels, leading to a sustained, nonspecific cationic current. Such a depolarizing current could induce cell automaticity and trigger the arrhythmic events during an early infarct when ATP/UTP release occurs. These results emphasize a new, potentially deleterious role of TRPC channel activation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Adenosine Triphosphate
Animals
Arrhythmias, Cardiac
Cell Membrane Permeability
Disease Models, Animal
Dogs
Estrenes
Humans
Male
Membrane Potentials
Mice
Mice, Knockout
Myocardial Infarction
Myocytes, Cardiac
Patch-Clamp Techniques
Phosphodiesterase Inhibitors
Phospholipase C beta
Pyrrolidinones
Rats
Rats, Wistar
Receptors, Purinergic P2
Signal Transduction
TRPC Cation Channels
Uridine Triphosphate
Megjelenés:American Journal of Physiology. Heart and Circulatory Physiology. - 295 (2008), p. H21-H28. -
További szerzők:Coulombe, Alaine Cazorla, Olivier Ugur, Mehmet Rauzier, Jean-Michel Magyar János (1961-) (élettanász) Mathieu, Eve-Lyne Boulay, Guylain Souto, Rafael Bideaux, Patrice Salazar, Guillermo Rassendren, Francois Lacampagne, Alain Fauconnier, Jérémy Vassort, Guy
Internet cím:DOI
elektronikus változat
Borító:

2.

001-es BibID:BIBFORM005623
Első szerző:Bagi Zsolt (orvos)
Cím:High intraluminal pressure via H2O2 upregulates arteriolar constrictions to angiotensin II by increasing the functional availability of AT1 receptors / Bagi, Z., Erdei, N., Koller, A.
Dátum:2008
ISSN:0363-6135 (Print)
Megjegyzések:Previously, we found that high intraluminal pressure leads to production of reactive oxygen species (ROS) and also upregulates several components of the renin-angiotensin system in the wall of small arteries. We hypothesized that acute exposure of arterioles to high intraluminal pressure in vitro via increasing ROS production enhances the functional availability of type 1 angiotensin II (Ang II) receptors (AT1 receptors), resulting in sustained constrictions. In arterioles ( approximately 180 mum) isolated from rat skeletal muscle, Ang II elicited dose-dependent constrictions, which decreased significantly by the second application [maximum (max.): from 59% +/- 4% to 26% +/- 5% at 10(-8) M; P < 0.05] in the presence of 80 mmHg of intraluminal pressure. In contrast, if the arterioles were exposed to high intraluminal pressure (160 mmHg for 30 min), Ang II-induced constrictions remained substantial on the second application (max.: 51% +/- 3% at 10(-8) M). In the presence of Tiron and polyethylene glycol (PEG)-catalase, known to reduce the level of superoxide anion and hydrogen peroxide (H(2)O(2)), second applications of Ang II evoked similarly reduced constrictions, even after high-pressure exposure (29% +/- 4% at 10(-8) M). Furthermore, when arterioles were exposed to H(2)O(2) (for 30 min, 10(-7) M, at normal 80 mmHg pressure), Ang II-induced constrictions remained substantial on second applications (59% +/- 5% at 10(-8) M). These findings suggest that high pressure, likely via inducing H(2)O(2) production, increases the functional availability of AT1 receptors and thus enhances Ang II-induced arteriolar constrictions. We propose that in hypertension-regardless of etiology-high intraluminal pressure, via oxidative stress, enhances the functional availability of AT1 receptors augmenting Ang II-induced constrictions.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt/pharmacology
Angiotensin II
Animals
Antioxidants
Arterioles
Blood Pressure
Catalase
Hydrogen Peroxide
Hypertension
Male
Muscle
Oxidative Stress
Polyethylene Glycols
Rats
Rats, Wistar
Receptor
Up-Regulation
Vasoconstriction/drug effects
Megjelenés:American Journal of Physiology. Heart and Circulatory Physiology. - 295 : 2 (2008), p. H835-H841. -
További szerzők:Erdei Nóra (1979-) (orvos) Koller Ákos
Internet cím:elektronikus változat
elektronikus változat
DOI
Borító:

3.

001-es BibID:BIBFORM029096
Első szerző:Bak István (vegyész, analitikus, farmakológus)
Cím:Cardioprotective mechanisms of Prunus cerasus (sour cherry) seed extract against ischemia-reperfusion-induced damage in isolated rat hearts / Bak I., Lekli I., Juhasz B., Nagy N., Varga E., Varadi J., Gesztelyi R., Szabo G., Szendrei L., Bacskay I., Vecsernyes M., Antal M., Fesus L., Boucher F., de Leiris J., Tosaki A.
Dátum:2006
Megjegyzések:The effects of kernel extract obtained from sour cherry (Prunus cerasus) seed on the postischemic cardiac recovery were studied in isolated working rat hearts. Rats were treated with various daily doses of the extract for 14 days, and hearts were then isolated and subjected to 30 min of global ischemia followed by 120 min of reperfusion. The incidence of ventricular fibrillation (VF) and tachycardia (VT) fell from their control values of 92% and 100% to 50% (not significant) and 58% (not significant), 17% (P<0.05), and 25% (P<0.05) with the doses of 10 mg/kg and 30 mg/kg of the extract, respectively. Lower concentrations of the extract (1 and 5 mg/kg) failed to significantly reduce the incidence of VF and VT during reperfusion. Sour cherry seed kernel extract (10 and 30 mg/kg) significantly improved the postischemic recovery of cardiac function (coronary flow, aortic flow, and left ventricular developed pressure) during reperfusion. We have also demonstrated that the extract-induced protection in cardiac function significantly reflected in a reduction of infarct size. Immunohistochemistry indicates that a reduction in caspase-3 activity and apoptotic cells by the extract, beside other potential action mechanisms of proanthocyanidin, trans-resveratrol, and flavonoid components of the extract, could be responsible for the cardioprotection in ischemic-reperfused myocardium.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:American Journal Of Physiology-Heart And Circulatory Physiology 291 : 3 (2006), p. H1329-H1336. -
További szerzők:Lekli István (1981-) (gyógyszerész) Juhász Béla (1978-) (kísérletes farmakológus) Nagy Norbert (1977-) (kísérletes farmakológus) Varga Edit (gyógyszerész) Váradi Judit (1973-) (gyógyszerész, gyógyszertechnológus) Gesztelyi Rudolf (1969-) (kísérletes farmakológus) Szabó Gergő Szendrei Levente Bácskay Ildikó (1969-) (gyógyszerész, gyógyszertechnológus) Vecsernyés Miklós (1959-) (gyógyszertechnológus, endokrinológus) Antal Miklós (1951-) (orvos, anatómus) Fésüs László (1947-) (orvos biokémikus) Boucher, Francois de Leiris, Joel Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

4.

001-es BibID:BIBFORM101050
Első szerző:Balasubramanian, Priya
Cím:Obesity-induced cognitive impairment in older adults : a microvascular perspective / Balasubramanian Priya, Kiss Tamas, Tarantini Stefano, Nyúl-Tóth Ádám, Ahire Chetan, Yabluchanskiy Andriy, Csipo Tamas, Lipecz Agnes, Tabak Adam, Institoris Adam, Csiszar Anna, Ungvari Zoltan
Dátum:2021
ISSN:0363-6135
Megjegyzések:Over two-thirds of individuals aged 65 and older are obese or overweight in the United States. Epidemiological data show an association between the degree of adiposity and cognitive dysfunction in the elderly. In this review, the pathophysiological roles of microvascular mechanisms, including impaired endothelial function and neurovascular coupling responses, microvascular rarefaction, and blood-brain barrier disruption in the genesis of cognitive impairment in geriatric obesity are considered. The potential contribution of adipose-derived factors and fundamental cellular and molecular mechanisms of senescence to exacerbated obesity-induced cerebromicrovascular impairment and cognitive decline in aging are discussed.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:American Journal Of Physiology-Heart And Circulatory Physiology. - 320 : 2 (2021), p. H740-H761. -
További szerzők:Kiss Tamás (1950-) (vegyész) Tarantini, Stefano Nyúl-Tóth Ádám Ahire, Chetan Yabluchanskiy, Andriy Csípő Tamás (1990-) Lipécz Ágnes Tabák Ádám Institóris Ádám Csiszár Anna Ungvári Zoltán
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

5.

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:

6.

001-es BibID:BIBFORM091835
Első szerző:Börzsei Denise
Cím:Exercise-mitigated sex-based differences in aging : from genetic alterations to heart performance / Denise Börzsei, Dániel Priksz, Renáta Szabó, Mariann Bombicz, Zoltán Karácsonyi, László G. Puskás, Liliána Z. Fehér, Zsolt Radák, Krisztina Kupai, Anikó Magyariné Berkó, Csaba Varga, Béla Juhász, Aniko Pósa
Dátum:2021
ISSN:0363-6135
Megjegyzések:The prevalence of cardiovascular diseases dramatically increases with age; therefore, striving to maintain a physiological heart function is particularly important. Our aim was to study the voluntary exercise-evoked cardioprotective effects in aged male and female rats, from genetic alterations to changes in heart performance. We divided 20-month-old female and male Wistar rats to control and running groups. After the 12-wk-long experimental period, echocardiographic measurements were performed. Afterwards, hearts were either removed for biochemical measurements or mounted into a Langendorff-perfusion system to detect infarct size. The following genes and their proteins were analyzed from heart: catechol-O-methyltransferase (Comt), endothelin-1 (Esm1), Purkinje cell protein-4 (Pcp4), and osteoglycin (Ogn). Recreational exercise caused functional improvements; however, changes were more prominent in males. Cardiac expression of Comt and Ogn was reduced as a result of exercise in aged males, whereas Pcp4 and Esm1 showed a marked overexpression, along with a markedly improved diastolic function. The key result of this study is that exercise enhanced the expression of the Pcp4 gene and protein, a recently described regulator of calcium balance in cardiomyocytes, and suppressed Comt and Ogn gene expression, which has been associated with impaired cardiac function. In addition, as a result of exercise, a significant improvement was observed in the size of infarct elicited by left anterior descending coronary artery occlusion. Our results clearly show that age and sex-dependent changes were both apparent in key proteins linked to cardiovascular physiology. Exercise-moderated fundamental genetic alterations may have contributed to the functional adaptation of the heart.NEW & NOTEWORTHY Voluntary exercise has proved to be an effective therapeutic tool to improve cardiac function in aged rats with clearly visible sex differences. Long-term exercise is associated with decreased Ogn and Comt expression and enhanced presence of Pcp4 and Esm1 genes. Sex-dependent changes were also observed in the expression of the cardiovascular key proteins. Fundamental alterations in gene and protein expression may contribute to the improvement of cardiac performance.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Pcp4
aging
echocardiography
exercise
gene expression
Megjelenés:American Journal Of Physiology-Heart And Circulatory Physiology. - 320 : 2 (2021), p. 854-866. -
További szerzők:Priksz Dániel (1989-) (farmakológus) Szabó Renáta Bombicz Mariann (1987-) (gyógyszerész) Karácsonyi Zoltán (1975-) (ortopéd és baleseti sebész) Puskás László G. Fehér Liliána Z. (Szeged) Radák Zsolt Kupai Krisztina Magyariné Berkó Anikó Varga Csaba (orvos) Juhász Béla (1978-) (kísérletes farmakológus) Pósa Anikó
Pályázati támogatás:GINOP-2.3.4-15-2016-00002
GINOP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

7.

001-es BibID:BIBFORM001086
Első szerző:Chen-Izu, Ye
Cím:Hypertension-induced remodeling of cardiac excitation-contraction coupling in ventricular myocytes occurs prior to hypertrophy development / Chen-Izu Y., Chen L., Bányász T., McCulle S. L., Norton B., Scharf S. M., Agarwal A., Patwardhan A., Izu L. T., Balke C. W.
Dátum:2007
ISSN:0363-6135 (Print)
Megjegyzések:Hypertension is a major risk factor for developing cardiac hypertrophy and heart failure. Previous studies show that hypertrophied and failing hearts display alterations in excitation-contraction (E-C) coupling. However, it is unclear whether remodeling of the E-C coupling system occurs before or after heart disease development. We hypothesized that hypertension might cause changes in the E-C coupling system that, in turn, induce hypertrophy. Here we tested this hypothesis by utilizing the progressive development of hypertensive heart disease in the spontaneously hypertensive rat (SHR) to identify a window period when SHR had just developed hypertension but had not yet developed hypertrophy. We found the following major changes in cardiac E-C coupling during this window period. 1) Using echocardiography and hemodynamics measurements, we found a decrease of left ventricular ejection fraction and cardiac output after the onset of hypertension. 2) Studies in isolated ventricular myocytes showed that myocardial contraction was also enhanced at the same time. 3) The action potential became prolonged. 4) The E-C coupling gain was increased. 5) The systolic Ca(2+) transient was augmented. These data show that profound changes in E-C coupling already occur at the onset of hypertension and precede hypertrophy development. Prolonged action potential and increased E-C coupling gain synergistically increase the Ca(2+) transient. Functionally, augmented Ca(2+) transient causes enhancement of myocardial contraction that can partially compensate for the greater workload to maintain cardiac output. The increased Ca(2+) signaling cascade as a molecular mechanism linking hypertension to cardiac hypertrophy development is also discussed.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Physiology. Heart and Circulatory Physiology 293 (2007), p. 3301-3310. -
További szerzők:Chen, L. Bányász Tamás (1960-) (élettanász) McCulle, S. L. Norton, Byron Scharf, S. M. Agarwal, Anupam Patwardhan, A. Izu, Leighton T. Balke, C. William
Internet cím:Elektronikus változat
DOI
Borító:

8.

001-es BibID:BIBFORM001084
Első szerző:Chen-Izu, Ye
Cím:Phosphorylation of RyR2 and shortening of RyR2 cluster spacing in spontaneously hypertensive rat with heart failure / Chen-Izu Y., Ward C. W., Stark W., Bányász T., Sumandea M. P., Balke W., Izu L. T., Wehrens X. H. T.
Dátum:2007
ISSN:0363-6135 (Print)
Megjegyzések:As a critical step toward understanding the role of abnormal intracellular Ca(2+) release via the ryanodine receptor (RyR(2)) during the development of hypertension-induced cardiac hypertrophy and heart failure, this study examines two questions: 1) At what stage, if ever, in the development of hypertrophy and heart failure is RyR(2) hyperphosphorylated at Ser(2808)? 2) Does the spatial distribution of RyR(2) clusters change in failing hearts? Using a newly developed semiquantitative immunohistochemistry method and Western blotting, we measured phosphorylation of RyR(2) at Ser(2808) in the spontaneously hypertensive rat (SHR) at four distinct disease stages. A major finding is that hyperphosphorylation of RyR(2) at Ser(2808) occurred only at late-stage heart failure in SHR, but not in age-matched controls. Furthermore, the spacing between RyR(2) clusters was shortened in failing hearts, as predicted by quantitative model simulation to increase spontaneous Ca(2+) wave generation and arrhythmias.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Physiology. Heart and Circulatory Physiology 293 (2007), p. 2409-2417. -
További szerzők:Ward, C. W. Stark, W. Bányász Tamás (1960-) (élettanász) Sumandea, M. P. Balke, C. William Izu, Leighton T. Wehrens, X. H. T.
Internet cím:elektronikus változat
DOI
Borító:

9.

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
DOI
Borító:

10.

001-es BibID:BIBFORM002023
Első szerző:Erdei Nóra (orvos)
Cím:H2O2 increases production of constrictor prostaglandins in smooth muscle leading to enhanced arteriolar tone in Type 2 diabetic mice / Erdei N., Bagi Z., Edes I., Kaley G., Koller A.
Dátum:2007
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal of Physiology. Heart and Circulatory Physiology. - 292 : 1 (2007), p. H649-H656. -
További szerzők:Édes István (1952-) (kardiológus) Kaley Gábor Koller Ákos Bagi Zsolt (1974-) (orvos)
Internet cím:elektronikus változat
DOI
Borító:

11.

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:

12.

001-es BibID:BIBFORM099988
Első szerző:Koller Ákos
Cím:Nitric oxide and H2O2 contribute to reactive dilation of isolated coronary arterioles / Koller Akos, Bagi Zsolt
Dátum:2004
ISSN:0363-6135
Megjegyzések:The role of metabolic factors derived from cardiac muscle in the development of reactive hyperemia after brief occlusions of the coronary circulation seems to be well established. However, the contribution of occlusion-induced changes in hemodynamic forces to eliciting reactive hyperemia is less known. We hypothesized that in isolated coronary arterioles changes in intraluminal pressure and flow, during and after release of occlusion (O/R), themselves via activating intrinsic mechanosensitive mechanisms, elicit release of vasoactive factors resulting in reactive dilations. Thus in isolated coronary arterioles (diameter: 88 +/- 8 microm) changes in diameter to changes in pressure or pressure plus flow (P+F) during and after a brief period (30, 60, and 120 s) of O/R of cannulating tube were measured by videomicroscopy. In response to both types of O/R, diameter first decreased, then, subsequently increased during occlusions. When only pressure was changed (from 80-10-80 mmHg), after release of occlusion, peak dilations increased as a function of the duration of occlusions. After flow was established (30 microl/min), O/R elicited changes in both pressure and flow (from 80-10-80 mmHg and from 0 to 30 microl/min). In these conditions, after the release of occlusions, not only the peak but also the duration of reactive dilation increased significantly as a function of the length of occlusions. The dilations during, and peak dilations after occlusions both in pressure and P+F protocols were significantly reduced by the inhibition of NO synthase with Nomega-nitro-L-arginine-methyl-ester (L-NAME) or by endothelium removal, whereas duration of postocclusion dilations were reduced by L-NAME or by endothelium removal only in P+F protocols. Furthermore, in both protocols, catalase significantly reduced the peak but not the duration of reactive dilations. Thus, mechanosensitive mechanisms that are sensitive to deformation, pressure, stretch, and wall shear stress elicit release of NO and H2O2, resulting in reactive dilation of isolated coronary arterioles.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:American Journal Of Physiology-Heart And Circulatory Physiology. - 287 : 6 (2004), p. H2461-H2467. -
További szerzők:Bagi Zsolt (1974-) (orvos)
Internet cím:DOI
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