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92. The influence of NO synthase inhibitor and free oxygen radicals scavenger - methylene Bblue - on streptozotocin induced diabetes in rats
- Creator:
- Haluzík, M., Nedvídková, J., and Škrha, J.
- Type:
- article, model:article, and TEXT
- Subject:
- diabetes, rat, oxidative stress, nitric oxide, superoxide dismutase, and malondialdehyde
- Language:
- English
- Description:
- The excessive production of nitric oxide (NO) and the subsequent increase of local oxidative stress is suggested as one of the pathophysiological mechanisms of streptozotocin-induced diabetes. It was reported that the administration of NO synthase inhibitors partially attenuated the development of streptozotocin-induced diabetes and reduced hyperglycaemia. Here we have studied the influence of methylene blue, which combines the properties of NO synthase inhibitor with antioxidant effects. The experiments were performed on male rats divided into four groups: control, diabetic (single dose of 70 mg of streptozotocin/kg i.p.), methylene blue (50 mg/kg in the food) and diabetic simultaneously fed with methylene blue. After 45 days the experiments were discontinued by decapitation. Serum glycaemia, glycated haemoglobin and oxidative stress parameters (plasma malondialdehyde concentration and erythrocyte superoxide dismutase activity) were significantly higher in the diabetic group. Simultaneous methylene blue administration partially reduced glycaemia and glycated haemoglobin, but did not decrease oxidative stress. We conclude that NO synthase inhibitor methylene blue partially attenuates the development of streptozotocin-induced diabetes in male rats, but does not reduce the development of oxidative stress in the diabetic group.
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
93. The influence of wine polyphenols on reactive oxygen and nitrogen species production by murine macrophages RAW 264.7
- Creator:
- Milan Číž, Martina Pavelková, Lucie Gallová, Jarmila Králová, Lukáš Kubala, and Antonín Lojek
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Obecná biologie, experimentální biologie, antioxidanty, polyfenoly, oxidační stres, oxid dusnatý, experimental biology, antioxidants, polyphenols, oxidative stress, nitric oxide, makrofágy, macrophages, 2, and 57
- Language:
- English
- Description:
- M. Číž, M. Pavelková, L. Gallová, J. Králová, L. Kubala, A. Lojek. and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
94. The interaction of endothelial nitric oxide synthase polymorphism and current smoking in terms of increased arterial stiffness
- Creator:
- Otto Mayer, Jan Filipovský, Martin Pešta, Renata Cífková, Milena Dolejšová, and Šimon, J.
- Format:
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, polymorfismus, kouření, nitric oxide, polymorphism, smoking, pulse wave velocity, nitric oxide synthase, T786C, G894T, 14, and 612
- Language:
- English
- Description:
- Nitric oxide belongs to the most important factors influencing structural and functional properties of vessel wall. Both genetic and environmental factors may influence its metabolism. The aim of this study was to explore whether two common polymorphisms of endothelial nitric synthase (eNOS) may, jointly with smoking, influence the stiffness of large arteries, quantified as pulse wave velocity (PWV). One hundred ninety four subjects free of manifest atherosclerotic disease or chronic pharmacotherapy were selected from population-based postMONICA study. PWV´s were measured using Sphygmocor® device between carotic and femoral arteries (aortic PWV) and between femoral and tibialis-posterior arteries (peripheral PWV). Two common polymorphisms, T786C and G894T, were assessed. Among current smokers, homo- or heterozygous carriers of T786C mutation showed significantly higher peripheral PWV than normal genotype carriers (14.0 vs 10.7 m/s, p<0.002); the same was true for the carriers of G894T mutation (13.9 vs 11.0 m/s, p<0.015). No differences were found in non-smokers, and neither of the eNOS polymorphisms influenced aortic PWV in our setting. In conclusion, genetically determined disorder of nitric oxide metabolism was associated with increased stiffness of peripheral, muscular-type arteries in generally healthy, untreated subjects, but only in the interaction with current smoking., O. Mayer jr. ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
95. The potential role of nitric oxide in the hypertrophic growth of the left ventricle
- Creator:
- Fedor Šimko and Šimko, J.
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, nitric oxide, cardiac hypertrophy, angiotensin II, L-NAME, 14, and 612
- Language:
- English
- Description:
- Left ventricular hypertrophy (LVH) is the result of interaction between a chronic hemodynamic overload and non-hemodynamic factors. There are several lines of evidence presented in this work suggesting that nitric oxide (NO) may participate in the hypertrophic growth of the myocardium. First, endothelial NO production was shown to be decreased in several types of hemodynamically overloaded circulation both in animals and humans. Second, compounds stimulating NO production were able to diminish the extent or modify the nature of LVH in some models of myocardial hypertrophic growth. Third, arterial hypertension can be induced by inhibition of nitric oxide synthase activity. This NO-deficient hypertension is associated with the development of concentric LVH, myocardial fibrosis and protein remodeling of the left ventricle. The mechanism of LVH development in NO-deficient hypertension is complex and involves decreased NO production and increased activation of the renin-angiotensin-aldosterone system. Cardiovascular protection via ACE inhibition in NO-deficient hypertension may be induced by mechanisms not involving an improvement of NO production. In conclusion, the hypertrophic growth of the LV appears to be the result of interaction of vasoconstrictive and growth stimulating effects of angiotensin II on the one hand and of vasodilating and antiproliferative effects of nitric oxide on the other., F. Šimko, J. Šimko., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
96. The restorative effect of apocynin and catalase in L-arginine induced hypotension on normotensive subjects – the role of oxidative stress
- Creator:
- Chia, Tan Yong, Murugaiyah, Vikneswaran, Sattar, Munavvar Abdul, Karim Khan, Nurzalina Abdul, Ahmad, Ashfaq, Abdulla, Mohammed Hadi, Johns, Edward James, Mei, Ho Yoke, Akhtar, Safia, and Ahmad, Fiaz Uddin
- Format:
- počítač and online zdroj
- Type:
- model:article and TEXT
- Subject:
- apocynin, catalase, L-arginine, nitric oxide, oxidative stress, and hypotension
- Language:
- English
- Description:
- L-arginine is a substrate for nitric oxide synthase (NOS) responsible for the production of NO. This investigation studied the effect of apocynin, an NADPH oxidase inhibitor and catalase, an H2O2 scavenger on L-arginine-induced oxidative stress and hypotension. Forty Wistar-Kyoto rats were treated for 14 days with vehicle, L-arginine (12.5 mg/ml p.o.), L-arginine + apocynin (2.5 mmol/l p.o.), L-arginine + catalase (10000 U/kg/day i.p.) and L-arginine plus apocynin + catalase respectively. Weekly renal functional and hemodynamic parameters were measured and kidneys harvested at the end of the study for histopathological and renal NADPH oxidase 4 (Nox4) assessments. L-arginine administration in normotensive rats decreased systolic blood pressure (120±2 vs. 91±2 mmHg) and heart rate (298±21 vs. 254±15 bpm), enhanced urinary output (21.5±4.2 vs. 32±1.9 ml/24 h, increased creatinine clearance (1.72±0.56 vs. 2.62±0.40 ml/min/kg), and fractional sodium excretion (0.88±0.16 vs. 1.18±0.16 %), caused proteinuria (28.10±1.93 vs. 35.26±1.69 mg/kg/day) and a significant decrease in renal cortical blood perfusion (292±3 vs. 258±5 bpu) and pulse wave velocity (3.72±0.20 vs 2.84±0.13 m/s) (all P<0.05). L-arginine increased plasma malondialdehyde (by ~206 % P<0.05) and NO (by ~51 %, P<0.05) but decreased superoxide dismutase (by ~31 %, P<0.05) and total antioxidant capacity (by ~35 %, P<0.05) compared to control. Renal Nox4 mRNA activity was approximately 2.1 fold higher (P<0.05) in the L-arginine-treated rats but was normalized by apocynin and apocynin plus catalase treatment. Administration of apocynin and catalase, but not catalase alone to rats fed L-arginine, restored the deranged renal function and structure, prevented hypotension and enhanced the antioxidant capacity and suppressed Nox4 expression. These findings suggest that apocynin and catalase might be used prophylactically in the states of oxidative stress.
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
97. The role of adrenergic agonists on glycogenolysis in rat hepatocyte cultures and possible involvement of NO
- Creator:
- Hodis, J., Nikolína Kutinová-Canová, Petr Potměšil, Ludmila Kameníková, Eva Kmoníčková, Zdeněk Zídek, and Hassan Farghali
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Experimentální medicína, farmakologie, oxid dusnatý, adrenalin, pharmacology, nitric oxide, adrenaline, glykogen, glykogenolýza, epinefrin, glycogen, glycogenolysis, epinephrine, iNOS, cAMP, 14, and 616-092
- Language:
- English
- Description:
- Certain liver metabolic diseases point to the presence of disturbances in glycogen deposition. Epinephrine raises the cAMP level that activates protein kinase A leading to the activation of phosphorylase and glycogen breakdown. In the present report, we sought to investigate whether NO is produced during adrenoceptor agonist-induced glycogenolysis in rat hepatocytes in cultures. Isolated glycogen rich rat hepatocytes in cultures were used. NO production (NO2-) was assessed under the effect of adrenergic agonists and adrenergic agonist/antagonist pairs, dibutyryl cyclic AMP sodium-potassium salt (db-cAMP), NO synthase (NOS) inhibitors Nω-nitro-L-arginine methyl ester (L-NAME), aminoguanidine (AG) and the NO donor S-nitroso-N-acetyl penicillamine (SNAP) . The inducible NO synthase (iNOS) mRNA was examined by the reverse transcription-polymerase chain reaction (RT-PCR). Glycogenolysis was quantified by glucose levels released into medium. The amount of glucose and NO2- released by hepatocytes was increased as a result of epinephrine, phenylephrine or db-cAMP treatments. The increase in glucose and NO2- released by epinephrine or phenylephrine was blocked or reduced by prazosin pretreatment and by NOS inhibitors aminoguanidine and L-NAME. iNOS gene expression was up-regulated by epinephrine. It can be concluded that glycogenolysis occurs through α adrenoceptor stimulation and a signaling cascade may involve NO production., J. Hodis, N. Kutinová-Canová, P. Potměšil, L. Kameníková, E. Kmoníčková, Z. Zídek, H. Farghali., and Obsahuje biblografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
98. The role of nitric oxide in the maintenance of vasoactive balance
- Creator:
- Oľga Pecháňová and Fedor Šimko
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, endoteliální dysfunkce, hypertenze, nitric oxide, endothelial dysfunction, hypertension, angiotensin II, endothelins, reactive oxygen species, 14, and 612
- Language:
- English
- Description:
- Endothelial dysfunction may be considered as the interstage between risk factors and cardiovascular pathology. An imbalance between the production of vasorelaxing and vasoconstricting factors plays a decisive role in the development of hypertension, atherosclerosis and target organ damage. Except vasorelaxing and antiproliferative properties per se, nitric oxide participates in antagonizing vasoconstrictive and growth promoting effects of angiotensin II, endothelins and reactive oxygen species. Angiotensin II is a potent activator of NAD(P)H oxidase contributing to the production of reactive oxygen species. Numerous signaling pathways activated in response to angiotensin II and endothelin-1 are mediated through the increased level of oxidative stress, which seems to be in casual relation to a number of cardiovascular disturbances including hypertension. With respect to the oxidative stress, the NO molecule seems to be of ambivalent nature. On the one hand, NO is able to reduce generation of reactive oxygen species by inhibiting association of NAD(P)H oxidase subunits. On the other hand, when excessively produced, NO reacts with superoxides resulting in the formation of peroxynitrite, which is a free radical deteriorating endothelial function. The balance between vasorelaxing and vasoconstricting substances appears to be the principal issue for the physiological functioning of the vascular bed., O. Pecháňová, F. Šimko., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
99. Vascular responses after long-term inhibition of nitric oxide synthesis in newborn dogs
- Creator:
- Török, J. and Gerová, M.
- Type:
- article, model:article, and TEXT
- Subject:
- newborn dogs, long-term inhibition, nitric oxide, endothelium-dependent relaxation, and neurogenic contraction
- Language:
- English
- Description:
- The effect of long-term inhibition of nitric oxide synthase on the relaxation and contraction ability of the thoracic aorta, carotid and pulmonary arteries was studied in the early postnatal period. Starting from the fifth day after birth, puppies were administered NG-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg/day subcutaneously) for 6 weeks. After this period, mean blood pressure increased from the control value of 94±14 mm Hg to 168±5 mm Hg (P<0.01) and the heart/body weight ratio from 6.22±0.25 to 8.23±0.45 (PcO.Ol). In control arterial rings precontracted by phenylephrine (10“5 mol/1), acetylcholine caused dose-dependent relaxations; the maximal values were reached in the range of 10 "8 to 10"* mol/1. In arteries from L-NAME treated puppies, acetylcholine also induced dose-dependent relaxations, the maximum values in the thoracic aorta (81.0±2.9 %) and carotid artery (87.2±6.9 %) were significantly reduced, not, however, in the pulmonary artery (76.4±7.8 %). Dose-response curves to acetylcholine in all the examined arteries from L-NAME-treated animals were shifted to the right indicating a decrease in sensitivity to acetylcholine. Neurogenic contractions, induced by electrical stimulation of adrenergic nerves, were not significantly altered in the thoracic aorta and carotid artery. However, in the pulmonary artery the contractions were greater at high frequency of stimulation. The findings that (i) submaximal doses of L-NAME attenuate acetylcholine-induced relaxation only slightly, and (ii) that it does not appreciably influence adrenergic contractions justify the hypothesis that the endothelium of vessels in newborn dogs is very probably endowed with a high content of nitric oxide synthase.
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public