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Start Over Subject Nitric oxide

22. Lack of reactive oxygen species deteriorates blood pressure regulation in acute stress

Creator:
Bernátová, I., Bališ, P., Goga, R., Behuliak, M., Zicha, J., and Sekaj, I.
Type:
article, model:article, and TEXT
Subject:
Air-jet stress, Superoxide, Nitric oxide, Sympathetic nervous system, and Renin-angiotensin system
Language:
English
Description:
This study investigated the contribution of reactive oxygen species (ROS) to blood pressure regulation in conscious adult male Wistar rats exposed to acute stress. Role of ROS was investigated in rats with temporally impaired principal blood pressure regulation systems using ganglionic blocker pentolinium (P, 5 mg/kg), angiotensin converting enzyme inhibitor captopril (C, 10 mg/kg), nitric oxide synthase inhibitor L-NAME (L, 30 mg/kg) and superoxide dismutase mimeticum tempol (T,25 mg/kg). Mean arterial pressure (MAP) was measured by the carotid artery catheter and inhibitors were administered intravenously. MAP was disturbed by a 3-s air jet, which increased MAP by 35.2±3.0 % vs. basal MAP after the first exposure. Air jet increased MAP in captopril- and tempol-treated rats similarly as observed in saline-treated rats. In pentolinium-treated rats stress significantly decreased MAP vs. pre -stressvalue. In L-NAME-treated rats stress failed to affect MAP significantly. Treatment of rats with P+L+C resulted in stress-induced MAP decrease by 17.3±1.3 % vs. pre-stress value and settling time (20.1±4.2 s). In P+L+C+T-treated rats stress led to maximal MAP decrease by 26.4±2.2 % (p<0.005 vs. P+L+C) and prolongation of settling time to 32.6±3.3 s (p<0.05 vs. P+L+C). Area under the MAP curve was significantly smaller in P+L+C-treated rats compared to P+L+C+T-treated ones (167±43 vs. 433±69 a.u., p<0.008). In conclusion, in rats with temporally impaired blood pressure regulation, the lack of ROS resulted in greater stress-induced MAP alterations and prolongation of time required to reach new post-stress steady state.
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23. Long-lasting Changes in the Density of Nitrergic Neurons Following Kainic Acid Administration and Chronic Hypoxia

Creator:
Benešová, P., Langmeier, M., Betka, J., and Trojan, S.
Type:
article, model:article, and TEXT
Subject:
Hypoxia, Kainic acid, Nitric oxide, Hippocampus, and Primary auditory cortex
Language:
English
Description:
Using histochemical analysis (NADPH-diaphorase) we have investigated the influence of intraperitoneal administration of kainic acid (KA), hypoxia and combination of both these factors on neurons of the hippocampus and on the primary auditory cortex (PAC) in male rats of the Wistar strain. Kainic acid was administered to 18-day-old animals, which were exposed to long-lasting repeated hypoxia from the 2nd till the 17th day of age in a hypobaric chamber (for 8 hours a day). At the age of 1 year, the animals were transcardially perfused with 4 % paraformaldehyde under deep thiopental anesthesia. Cryostate sections were stained to identify NADP H-diaphorase positive neurons that were then quantified in CA1 and CA3 areas of the hippocampus, in the dentate gyrus and in the PAC. Both, hypoxia and KA lowered the number of NADPH-diaphorase positive neurons in the hilus, dorsal and ventral blades of the dentate gyrus, CA1 and CA3 areas of the hippocampus. On the contrary, KA given to the hypoxic animals increased the number of NADPH-diaphorase positive neurons in the dorsal blade of the dentate gyrus and PAC.
Rights:
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24. Nitric oxide participates in IFN-γ-induced HUVECs hyperpermeability

Creator:
Ng, C.T., Fong, L.Y., Low, Y.Y., Ban, J., Hakim, M.N., and Ahmad, Z.
Type:
article, model:article, and TEXT
Subject:
Interferon-gamma, Permeability, Human umbilical vein endothelial cells, Nitric oxide, and Cyclic guanosine monophosphate
Language:
English
Description:
The endothelial barrier function is tightly controlled by a broad range of signaling cascades including nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway. It has been proposed that disturbances in NO and cGMP production could interfere with proper endothelial barrier function. In this study, we assessed the effect of interferon-gamma (IFN-γ), a pro-inflammatory cytokine, on NO and cGMP levels and examined the mechanisms by which NO and cGMP regulate the IFN-γ-mediated HUVECs hyperpermeability. The flux of fluorescein isothiocyanate-labeled dextran across cell monolayers was used to study the permeability of endothelial cells. Here, we found that IFN-γ significantly attenuated basal NO concentration and the increased NO levels supplied by a NO donor, sodium nitroprusside (SNP). Besides, application of IFN-γ also significantly attenuated both the basal cGMP concentration and the increased cGMP production donated by a cell permeable cGMP analogue, 8-bromo- cyclic GMP (8-Br-cGMP). In addition, exposure of the cell monolayer to IFN -γ significantly increased HUVECs basal permeability. However, L-NAME pretreatment did not suppress IFN-γ-induced HUVECs hyperpermeability. L- NAME pretreatment followed by SNP or SNP pretreatment partially reduced IFN-γ-induced HUVECs hyperpermeability. Pretreatment with a guanylate cyclase inhibitor, 6-anilino-5,8-quinolinedione (LY83583), led to a further increase in IFN-γ-induced HUVECs hyperpermeability. The findings suggest that the mechanism underlying IFN-γ-induced increased HUVECs permeability is partly related to the inhibition of NO production.
Rights:
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25. Organ Microcirculatory Disturbances in Experimental Acute Pancreatitis. A Role of Nitric Oxide

Creator:
Dobosz, M., Hac, S., Mionskowska, L., Dymecki, D., Dobrowolski, S., and Wajda, Z.
Type:
article, model:article, and TEXT
Subject:
Acute pancreatitis, Microcirculation, and Nitric oxide
Language:
English
Description:
Microcirculatory disturbances are important early pathophysiological events in various organs during acute pancreatitis (AP). The aim of the study was to investigate an influence of L-arginine (nitric oxide substrate) and NG-nitro-L-arginine (L-NNA, nitric oxide synthase inhibitor) on organ microcirculation in experimental acute pancreatitis induced by four consecutive intraperitoneal cerulein injections (15 μg/kg/h). The microcirculation of pancreas, liver, kidney, stomach, colon and skeletal muscle was measured by laser Doppler flowmeter. Serum interleukin 6 and hematocrit levels were analyzed. AP resulted in a significant drop of microperfusion in all examined organ. L-arginine administration (2x100 mg/kg) improved the microcirculation in the pancreas, liver, kidney, colon and skeletal muscle, and lowered hematocrit levels. L-NNA treatment (2x25 mg/kg) caused aggravation of edematous AP to the necrotizing situation, and increased IL-6 and hematocrit levels. A further reduction of blood perfusion was noted in the stomach only. It is concluded that L-arginine administration has a positive influence on organ microcirculatory disturbances accompanying experimental cerulein-induced AP. NO inhibition aggravates the course of pancreatitis.
Rights:
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26. 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:
print, bez média, and svazek
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:
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27. Systemic blood pressure response to the inhibition of two hyperpolarizing pathways: a comparison to NO-synthase inhibition

Creator:
Gerová, M. and Kittová, M.
Type:
article, model:article, and TEXT
Subject:
Hyperpolarizing factors, Nitric oxide, Systemic blood pressure, Hypertension, Acetylcholine, and Bradykinin
Language:
English
Description:
The impact on blood pressure of two vasodilating mechanisms, underlied by vascular smooth muscle hyperpolarization, was studied and compared to that induced by nitric oxide (NO) mechanism. Systemic blood pressure, after inhibitory intervention in arachidonic acid metabolism (cytochrome P-450 inhibition by miconazole 0.5 mg/100 g b.w.), one of the hyperpolarizing pathways, did not change. After the inhibition of the action voltage-dependent K+ channels operator (by 4-aminopyridine 0.1 mg/100 g b.w.) , the other hyperpolarizing pathway, blood pressure declined slightly (from 132.3±3.2 mm Hg to 116.5±5.0 mm Hg, P<0.05). Inhibition of nitric oxide production (L-NAME 5 mg/100 g b.w.) increased blood pressure considerably (123.5±2.7 mm Hg to 155.4±3.1 mm Hg, P<0.001). After inhibition of the hyperpolarizing pathway by miconazole, hypotension induced by acetylcholine (Ach, 10 μg) represented 63.0±1.9 mm Hg vs control value 78.6±5.2 mm Hg (P<0.001), by bradykinin (BK) (100 μg) 59.4±3.9 mm Hg vs control value 71.2±6.1 mm Hg (P<0.05). After inhibition of the hyperpolarizing pathway by 4-aminopyridine, hypotension induced by ACh (10 μg) achieved 64.6±2.5 mm Hg vs control value 78.4±2.8 mm Hg (P<0.001) and that induced by BK (100 μg) 56.6±5.3 mm Hg vs control value 72.3±2.5 mm Hg (P<0.001). ACh or BK hypotension after the inhibition of the above hyperpolarizing pathways was significantly attenuated. On the contrary, after NO-synthase inhibition the hypotension to ACh was significantly enhanced. Blood pressure decrease after ACh (10 μg) hypotension was 91.8±4.1 mm Hg vs control value 79.3±3.3 mm Hg (P<0.01), and after BK (100 μg) it was 78.4±7.1 mm Hg vs control value 68.3±5.2 mm Hg. A different basal BP response, but equally attenuated hypotension to Ach and BK, was detected after the inhibition of two selected hyperpolarizing pathways. In cotrast, the inhibition of NO production elicited an increase in systemic BP and augmentation of ACh and BK hypotension. The effectiveness of further hyperpolarizing mechanisms in relation to systemic BP regulation and nitric oxide level remains open.
Rights:
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28. The absence of sympathoexcitation during the development of hypertension in Cyp1a1 Ren-2 transgenic rats

Creator:
Zicha, J. , Hojná, S., Kopkan, L. , Červenka, L. , and Vaněčková, I.
Format:
bez média and svazek
Type:
model:article and TEXT
Subject:
Indole-3 carbinol, Blood pressure, Angiotensin II, Sympathetic nervous system, Nitric oxide, Rho kinase pathway, and Fasudil
Language:
English
Description:
The insertion of mouse renin gene (Ren-2) into the genome of normotensive rats causes a spontaneous rise of blood pressure (BP), leading to an angiotensin II (Ang II)-dependent form of hypertension in transgenic (mRen-2)27 rats (TGR). However, enhanced sympathetic BP component was demonstrated in heterozygous TGR aged 20 weeks. In the present study we used another model, i.e. Cyp1a1-Ren-2 transgenic rats (iTGR) in which hypertension can be induced by natural xenobiotic indole-3 carbinol (I3C) added to the diet. We investigated whether the development of high blood pressure (BP) in 5-month-old iTGR animals fed I3C diet for 10 days is solely due to enhanced Ang II-dependent vasoconstriction or whether enhanced sympathetic vasoconstriction also participates in BP maintenance in this form of hypertension. Using acute sequential blockade of renin-angiotensin system (RAS), sympathetic nervous system (SNS) and NO synthase (NOS) we have demonstrated that the observed gradual increase of BP in iTGR fed I3C diet was entirely due to the augmentation of Ang II-dependent BP component without significant changes of sympathetic BP component. Thus, the hypertension in iTGR resembles to that of homozygous TGR in which high BP was entirely dependent on Ang II-dependent vasoconstriction. Moreover, our measurements of acute BP response to Rho kinase inhibitor fasudil in animals subjected to a combined blockade of RAS, SNS and NOS indicated the attenuation of basal calcium sensitization in both iTGR and homozygous TGR.
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29. The Effects of Nitroglycerine on the Redox Status of Rat Erythrocytes and Reticulocytes

Creator:
Marković, S.D., Ognjanović, B.I., Štajn , A.Š., Žikić, R.V. , Saičić, Z.S., Radojičić, R.M., and Spasić, M.B.
Type:
article, model:article, and TEXT
Subject:
Erythrocytes, Nitric oxide, Nitroglycerine, Oxidative stress, and Reticulocytes
Language:
English
Description:
The effects of nitroglycerine (NTG) are mediated by liberated nitric oxide (NO) after NTG enzymatic bio-transformation in cells. The aim of this study was to evaluate some products of NTG bio-transformation and their consequences on the redox status of rat erythrocytes and reticulocytes, considering the absence and presence of functional mitochondria in these cells, respectively. Rat erythrocyte and reticulocyte-rich red blood cell (RBC) suspensions were aerobically incubated (2 h, 37 0C) without (control) or in the presence of different concentrations of NTG (0.1, 0.25, 0.5, 1.0 and 1.5 mM). In rat erythrocytes, NTG did not elevate the concentrations of any reactive nitrogen species (RNS). However, NTG robustly increased concentration of methemoglobin (MetHb), suggesting that NTG bio-transformation was primarily connected with hemoglobin (Hb). NTG-induced MetHb formation was followed by the induction of lipid peroxidation. In rat reticulocytes, NTG caused an increase in the levels of nitrite, peroxinitrite, hydrogen peroxide, MetHb and lipid peroxide levels, but it decreased the level of the superoxide anion radical. Millimolar concentrations of NTG caused oxidative damage of both erythrocytes and reticulocytes. These data indicate that two pathways of NTG bio-transformation exist in reticulocytes: one generating RNS and the other connected with Hb (as in erythrocytes). In conclusion, NTG bio-transformation is different in erythrocytes and reticulocytes due to the presence of mitochondria in the latter.
Rights:
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30. The role of hydrogen sulphide in blood pressure regulation

Creator:
Cacanyiova, S., Berenyiova, A., and Kristek, F.
Type:
article, model:article, and TEXT
Subject:
Hydrogen sulphide, Nitric oxide, Vascular tone, Hypertension, and Nitro-sulphide
Language:
English
Description:
Cardiovascular studies have confirmed that hydrogen sulphide (H2S) is involved in various signaling pathways in both physiological and pathological conditions, including hypertension. In contrast to nitric oxide (NO), which has a clear vasorelaxant action, H2S has both vasorelaxing and vasoconstricting effects on the cardiovascular system. H2S is an important antihypertensive agent, and the reduced production of H2S and the alterations in its functions are involved in the initiation of spontaneous hypertension. Moreover, cross-talk between H2S and NO has been reported. NO-H2S interactions include reactions between the molecules themselves, and each has been shown to regulate the endogenous production of the other. In addition, NO and H2S can interact to form a nitrosothiol/s complex, which has original properties and represents a novel nitroso-sulphide signaling pathway. Furthermore, recent results have shown that the interaction between H2S and NO could be involved in the endothelium-regulated compensatory mechanisms that are observed in juvenile spontaneously hypertensive rats. The present review is devoted to role of H2S in vascular tone regulation. We primarily focus on the mechanisms of H2S-NO interactions and on the role of H2S in blood pressure regulation in normotensive and spontaneously hypertensive rats.
Rights:
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