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12. Long-term administration of D-NAME induces hemodynamic and structural changes in the cardiovascular system
- Creator:
- Pavel Babál, Oľga Pecháňová, and Iveta Bernátová
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- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, hypertenze, hypertension, nitric oxide synthase, L-NAME, D-NAME, myocardial fibrosis, arterial hyperplasia, 14, and 612
- Language:
- English
- Description:
- NG-nitro-D-arginine-methyl ester (D-NAME) is considered to be an inactive enantiomer of L-NAME and is generally used as the negative control for NO synthase inhibition with L-NAME. With the aim to compare the effects of 4-week L-NAME and D-NAME treatments on hemodynamic and cardiovascular structural parameters, four groups of male Wistar rats were investigated: the controls and groups administered 40 and 20 mg/kg/day of L-NAME and 40 mg/kg/day of D-NAME. At the end of the experiment, myocardial NO synthase activity decreased by 42, 24 and 25 %; aortic NO synthase activity decreased by 35, 15 and 13 % vs. controls in the L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. The DNA concentrations in the myocardium and the aorta increased significantly after L-NAME and D-NAME treatments. The inhibition of NO synthase was accompanied by a significant elevation in systolic blood pressure in all three groups. The LVW/BW ratio increased by 27, 14 and 13 % vs. controls in the L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. The aortic wall mass, measured as the crossectional area, increased by 45, 17 and 25 % vs. controls in the L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. Myocardial fibrosis represented 0.94 % in the controls, but 7.96, 4.70 and 5.25 % in L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. It is concluded that D-NAME, although less affective than L-NAME, inhibits NO synthase activity resulting in hemodynamic and structural changes in the cardiovascular system similar to the changes induced by half the dose of L-NAME. Thus, the consideration of D-NAME as an inactive enantiomer and its use as the negative control needs to be reevaluated., P. Babál, O. Pecháňová, I. Bernátová., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
13. Morphological alterations and NO-synthase expression in heart after continuous light exposure of rats
- Creator:
- Ľudovít Paulis, Važan, R., Fedor Šimko, Oľga Pecháňová, Ján Styk, Pavel Babál, and Pavol Janega
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- Subject:
- Fyziologie člověka a srovnávací fyziologie, myokard, melatonin, myocardium, fibrosis collagen I/II, nitric oxide synthase, 14, and 612
- Language:
- English
- Description:
- Although exposure to continuous light is associated with hypertension and modulates the outcome of ischemiareperfusion injury, less attention has been paid to its effects on cardiac morphology. We investigated whether 4-week exposure of experimental rats to continuous 24 h/day light can modify cardiac morphology, with focus on heart weight, fibrosis and collagen I/III ratio in correlation with NO-synthase expression. Two groups of male adult Wistar rats were studied: controls exposed to normal light/dark cycle (12 h/day light, 12 h/day dark) and rats exposed to continuous light. After 4 weeks of treatment the absolute and the relative heart weights were determined and myocardial fibrosis and collagen type I/III ratio were evaluated using picrosirius red staining. Endothelial and inducible NO-synthase expression was detected immunohistochemically. The exposure of rats to continuous light resulted in an increase of body weight with proportionally increased heart weight. Myocardial fibrosis remained unaffected but collagen I/III ratio increased. Neither endothelial nor inducible NO-synthase expression was altered in light-exposed rats. We conclude that the loss of structural homogeneity of the myocardium in favor of collagen type I might increase myocardial stiffness and contribute to functional alterations after continuous light exposure., L'. Paulis, R. Važan, F. Šimko, O. Pecháňová, J. Styk, P. Babál, P. Janega., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
14. Red wine polyphenols affect the collagen composition in the aorta after oxidative damage induced by chronic administration of CCl4
- Creator:
- Hlavačková, L., Pavol Janega, Andrea Černá, Oľga Pecháňová, Ramaroson Andriantsitohaina, and Pavel Babál
- Format:
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, červená vína, polyfenoly, kolagen, aorta, tetrachlormethan, physiology, red wine, polyphenols, collagen, carbon tetrachloride, 14, and 612
- Language:
- English
- Description:
- Increased amount of collagen type I and decreased amount of type III is described in various pathological processes in the vascular wall. Polyphenols were shown to have protective effect on endothelium, decrease blood pressure and prevent oxidative damage induced by various stimuli. Tetrachlormethane (CCl4) is a toxic substance with known negative systemic effects induced by free radicals. Chronic administration of CCl4 for 12 weeks led to an increase of collagen type I and a decrease of type III in the wall of aorta. Parallel administration of red wine polyphenols significantly reduced the increase of collagen type I, at the same time the content of type III rose to the level above controls. After 4 weeks of spontaneous recovery no changes were observed. If polyphenols were administered during the recovery period, there was a decrease of type I and an increase of type III collagen content in the aorta. It can be concluded that polyphenols have a tendency to lower the amount of type I and to increase the proportion of type III collagen in the wall of the aorta. These changes are significant in prevention or in regression of changes induced by chronic oxidative stress. This effect of polyphenols is most likely the result of their influence on MMP-1 and TIMP activities through which they positively influence the collagen types I and III content ratio in the vascular wall in favor of the type III collagen., L. Hlavačková ... [et al.]., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
15. Red wine polyphenols induce vasorelaxation via increased nitric oxide bioactivity
- Creator:
- Zenebe, W., Oľga Pecháňová, and Ramaroson Andriantsitohaina
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- Subject:
- Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, volné radikály, endotel, nitric oxide, free radicals, endothelium, red wine polyphenolic compounds, free oxygen radicals, femoral artery, 14, and 612
- Language:
- English
- Description:
- The aim of the present study was to investigate the mechanism of vasorelaxant responses induced by red wine polyphenolic compounds (Provinol). Rings of rat femoral artery with or without functional endothelium were set up in a myograph for isometric recording and precontracted with phenylephrine (10-5 M). Provinol in cumulative doses (10-9 to 10-3 mg/ml) elicited endothelium- and dose-dependent relaxation of the artery with maximal relaxation of 56 % at the concentration of 10-5 mg/ml. The relaxant responses to Provinol correlated well with the increase of NO synthase activity in the vascular tissue after administration of cumulative doses of Provinol (10-9 to 10-3 mg/ml). NG-nitro-L-arginine methylester (L-NAME, 3x10-4 M) significantly attenuated the endothelium-dependent relaxation produced by Provinol. Administration of L-arginine (3x10-5 M) restored the relaxation inhibited by L-NAME. The relaxant responses of Provinol were abolished in the presence of Ca2+-entry blocker, verapamil (10-6 M). Administration of hydrogen peroxide (H2O2) abolished acetylcholine (10-5 M)-induced relaxation of the rat femoral artery, while administration of Provinol (10-5 mg/ml) together with H2O2 helped to maintain the acetylcholine-induced relaxation. Provinol only partially affected the concentration-response curve for the NO donor sodium nitroprusside-induced relaxation in rings without endothelium. In conclusion, Provinol elicited endothelium-dependent relaxation of rat femoral artery by the Ca2+-induced increase of NO synthase activity and by protecting NO from degradation., W. Zenebe, O. Pecháňová, R. Andriantsitohaina., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
16. Red wine polyphenols prevent cyclosporine-induced nephrotoxicity at the level of the intrinsic apoptotic pathway
- Creator:
- Rezzani, R., Tengattini, S., Bonomini, F., Filippini, F., Oľga Pecháňová, Bianchi, R., and Ramaroson Andriantsitohaina
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, imunohistochemie, apoptóza, nefrotoxicita, nemoci ledvin, immunohistochemistry, apoptosis, nephrotoxicity, kidney diseases, cyclosporine nephrotoxicity, ProvinolsTM, 14, and 612
- Language:
- English
- Description:
- Flavonoids, polyphenol derivatives of plant origin, possess a broad range of pharmacological properties. A number of studies have found both pro/anti-apoptotic effects for many of these compounds. For these reasons we investigated whether ProvinolsTM, flavonoids obtained from red wine, have anti-apoptotic properties. The investigations have been carried out in rats treated with Cyclosporine A (CsA). In particular, four groups of rats have been treated for 21 days with either olive oil (control group), with CsA, with ProvinolsTM, or with CsA and ProvinolsTM simultaneously. Oxidative stress, systolic blood pressure, body weight, biochemical parameters and different markers of pro/anti-apoptotic pathway were measured. CsA produced an increase of systolic blood pressure, a decrease in body weight, serum creatinine levels, urinary total protein concentration and creatinine clearance. Moreover, CsA induced renal alterations and the translocation of Bax and cytochrome c from cytoplasm to mitochondria and vice versa. These changes activated the caspase cascade pathway, that leads to morphological and biochemical features of apoptosis. ProvinolsTM restored morphological and biochemical alterations and prevented nephrotoxicity. In conclusion, this study may augment our current understanding of the controversial pro-/anti-apoptotic properties of flavonoids and their molecular mechanisms., R. Rezzani ... [et al.]., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
17. Regulatory role of nitric oxide on the cardiac Na, K-ATPase in hypertension
- Creator:
- Vlkovičová, J., Veronika Javorková, Mézešová, L., Oľga Pecháňová, and Vrbjar, Norbert
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- Subject:
- Fyziologie člověka a srovnávací fyziologie, kardiovaskulární fyziologie, hypertenze, oxid dusnatý, srdce, cardiovascular physiology, hypertension, nitric oxide, heart, sodium pump, 14, and 612
- Language:
- English
- Description:
- The present study was focused on regulatory role of nitric oxide on functional properties of the cardiac Na, K-ATPase in three various animal models of hypertension: spontaneously hypertensive male rats (SHR) with increased activity of nitric oxide synthase (NOS) by 60 % (Sh1), SHR with decreased activity of NOS by 40 % (Sh2) and rats with hypertension induced by L-NAME (40 mg/kg/day) with depressed activity of NOS by 72 % (LN). Studying the utilization of energy substrate we observed higher Na, K-ATPase activity in the whole concentration range of ATP in Sh1 and decreased activity in Sh2 and LN. Evaluation of kinetic parameters revealed an increase of Vmax value by 37 % in Sh1 and decrease by 30 % in Sh2 and 17 % in LN. The KM value remained unchanged in Sh2 and LN, but was lower by 38 % in Sh1 indicating increased affinity of the ATP binding site, as compared to controls. During the activation with Na+ we observed increased Vmax by 64 % and increased KNa by 106 % in Sh1. In Sh2 we found decreased Vmax by 40 % and increased KNa by 38 %. In LN, the enzyme showed unchanged Vmax with increased KNa by 50 %. The above data indicate a positive role of increased activity of NOS in improved utilization of ATP as well as enhanced binding of Na+ by the cardiac Na, K-ATPase., J. Vlkovičová, V. Javorková, L. Mézešová, O. Pecháňová, N. Vrbjar., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
18. Short-term administration of alibernet red wine extract failed to affect blood pressure and to improve endothelial function in young normotensive and spontaneously hypertensive rats
- Creator:
- Bališ, P., Angelika Púzserová, Peter Slezák, Šestáková, N., Oľga Pecháňová, and Bernátová, I.
- Format:
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, antioxidanty, krevní tlak, antioxidants, blood pressure, nitric oxide, endothelial function, red wine polyphenols, 14, and 612
- Language:
- English
- Description:
- As wine polyphenols were show n to possess many positive effects in mammals, including improvement of vascular function, this study investigated the effect of the Slovak Alibernet red wine extract (AWE) on blood pressure and vascular function in young normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Six weeks old, male, WKY and SHR were treated with AWE for three weeks at the dose of 24.2 mg/kg/day. Blood pressure (BP), determined by tail-cuff plethysmography, was significantly elevated in SHR vs. WKY and AWE failed to affect it. Lipid peroxidation was evaluated by determination of thiobarbituric acid-reactive substances. Vascular function was assessed in rings of the femoral artery using Mulvany-Halpern’s myograph. Maximal endothelium-dependent acetylcholine (ACh)-induced rela xation was reduced in control SHR vs. WKY rats by approximatel y 9.3 %, which was associated with a significant decrease of its NO-independent component. AWE failed to affect maximal AC h-induced relaxation, both its NO-dependent and independen t components, compared to controls of the same genotype. AWE however reduced lipid peroxidation in the left ventricle of both WKY and SHR and in the liver of SHR. In conclusion, three-week administration of AWE failed to reduce BP and to improve endothelial function in the femoral arteries of both genotypes investigated., P. Bališ ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
19. Short-term NO Synthase Inhibition and the ATP Affinity of Cardiac Na,K-ATPase
- Creator:
- Vrbjar, N., Monika Ivanová, Oľga Pecháňová, and Mária Gerová
- Format:
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- Type:
- article, studie, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, Sodium pump, Heart, Pressure overload, Nitric oxide, L-NAME, 14, and 612
- Language:
- English
- Description:
- It was previously shown that 4 hours´ lasting inhibition of nitric oxide synthesis by administration of an L-arginine analogue, the NG-nitro-L-arginine methyl ester (L-NAME) changed the affinity of the Na-binding site of Na,K-ATPase thus resulting in elevation of enzyme activity especially at higher concentrations of sodium. Using the same experimental model, we focused our attention in the present study to the question of binding of ATP to the enzyme molecule in the left ventricle (LV), ventricular septum (S) and the right ventricle (RV) of the dog heart. Activation of the enzyme by increasing concentrations of ATP revealed a significant increase of the Vmax only in septum (by 38 %). The KM increased significantly in septum (by 40 %) and in left ventricle (by 56 %) indicating an altered sensitivity of the ATP-binding site of Na,K-ATPase in the hearts of NO-deficient animals. The alterations of Na,K-ATPase in its ability to bind and hydrolyze ATP are localized to the tissue surrounding the cavity of the left ventricle., N. Vrbjar, M. Strnisková, O. Pecháňová, M. Gerová., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
20. Short-term NO synthase inhibition and the Na+ - binding properties of cardiac Na,K-ATPase
- Creator:
- Vrbjar, N., Monika Ivanová, Oľga Pecháňová, and Mária Gerová
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, srdce, oxid dusnatý, heart, nitric oxide, pressure overload, L-NAME, 14, and 612
- Language:
- English
- Description:
- It is known that hypertension is accompanied by increased [Na+]i. The functional properties of Na,K-ATPase, which transports the Na+ out and K+ into myocardial cells during the relaxation phase, were investigated in the left ventricle (LV), septum (SV) and the right ventricle (RV) of anesthetized dogs with moderate acute blood pressure elevation elicited by short-term (4-hour) NO synthase inhibition. The NO-insufficiency was induced by administration of an L-arginine analogue, the NG-nitro-L-arginine methyl ester (L-NAME). Concerning the function of Na,K-ATPase under the conditions of lowered NO synthesis, we focused our attention to the binding of Na+ to the enzyme molecule. Activation of the enzyme by increasing Na+ concentrations revealed significant changes in both the maximal velocity (Vmax) and the affinity for Na+ (KNa) in all investigated heart sections. The Vmax increased by 27 % in LV, by 87 % in SV and by 58 % in RV. The KNa value increased by 86 % in LV, by 105 % in SV and by 93% in RV, indicating an apparent decrease in the sensitivity of the Na+-binding site in the Na,K-ATPase molecule. This apparently decreased pump affinity for Na+ together with the increase of Vmax suggest that, during the short-term inhibition of NO synthesis, the Na,K-ATPase is capable of extruding the excessive Na+ from the myocardial cells more effectively at higher [Na+]i as compared to the Na,K-ATPase of control animals., N. Vrbjar, M. Strnisková, O. Pecháňová, M. Gerová., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
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