scholarly journals Nitric Oxide Protects L-Type Calcium Channel of Cardiomyocyte during Long-Term Isoproterenol Stimulation in Tail-Suspended Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Zhi-Jie Yue ◽  
Peng-Tao Xu ◽  
Bo Jiao ◽  
Hui Chang ◽  
Zhen Song ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Calcium Channel ◽  
Calcium Current ◽  
Specific Inhibitor ◽  
Oxygen Species ◽  
Similar Extent ◽  
Initial Value ◽  
No Donor ◽  
Expression And Activity

The aim of this study was to investigate the effects of nitric oxide (NO) and reactive oxygen species (ROS) on L-type calcium channel (LTCC) gating properties of cardiomyocytes during long-term isoproterenol (ISO) stimulation. Expression and activity of nNOS as well asS-nitrosylation of LTCCα1C subunit significantly decreased in the myocardium of SUS rats. Long-term ISO stimulation increased ROS in cardiomyocytes of SUS rats. ISO-enhanced calcium current (ICa,L) in the SUS group was less than that in the CON group. The maximalICa,Ldecreased to about 80% or 60% of initial value at the 50th minute of ISO treatment in CON or SUS group, respectively. Specific inhibitor NAAN of nNOS reduced maximalICa,Lto 50% of initial value in the CON group; in contrast, NO donor SNAP maintained maximalICa,Lin SUS group to similar extent of CON group after 50 min of ISO treatment. Long-term ISO stimulation also changed steady-state activation (P<0.01), inactivation (P<0.01), and recovery (P<0.05) characteristics of LTCC in SUS group. In conclusion, NO-inducedS-nitrosylation of LTCCα1C subunit may competitively prevent oxidation from ROS at the same sites. Furthermore, LTCC can be protected by NO during long-term ISO stimulation.

Effect of extracellular Mg2+ on ROS and Ca2+ accumulation during reoxygenation of rat cardiomyocytes

2001 ◽  
Vol 280 (1) ◽  
pp. H344-H353 ◽  
Author(s):  
Mohammad N. Sharikabad ◽  
Kirsten M. Østbye ◽  
Torstein Lyberg ◽  
Odd Brørs
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Flow Cytometry ◽  
Lactate Dehydrogenase ◽  
Superoxide Anion ◽  
Oxygen Species ◽  
No Donor ◽  
Rat Cardiomyocytes ◽  
Intracellular Ros ◽  
Ldh Release

The effects of Mg2+ on reactive oxygen species (ROS) and cell Ca2+ during reoxygenation of hypoxic rat cardiomyocytes were studied. Oxidation of 2′,7′-dichlorodihydrofluorescein (DCDHF) to dichlorofluorescein (DCF) and of dihydroethidium (DHE) to ethidium (ETH) within cells were used as markers for intracellular ROS levels and were determined by flow cytometry. DCDHF/DCF is sensitive to H2O2 and nitric oxide (NO), and DHE/ETH is sensitive to the superoxide anion (O2 −·), respectively. Rapidly exchangeable cell Ca2+ was determined by 45Ca2+uptake. Cells were exposed to hypoxia for 1 h and reoxygenation for 2 h. ROS levels, determined as DCF fluorescence, were increased 100–130% during reoxygenation alone and further increased 60% by increasing extracellular Mg2+concentration to 5 mM at reoxygenation. ROS levels, measured as ETH fluorescence, were increased 16–24% during reoxygenation but were not affected by Mg2+. Cell Ca2+ increased three- to fourfold during reoxygenation. This increase was reduced 40% by 5 mM Mg2+, 57% by 10 μM 3,4-dichlorobenzamil (DCB) (inhibitor of Na+/Ca2+ exchange), and 75% by combining Mg2+ and DCB. H2O2 (25 and 500 μM) reduced Ca2+ accumulation by 38 and 43%, respectively, whereas the NO donor S-nitroso- N-acetyl-penicillamine (1 mM) had no effect. Mg2+ reduced hypoxia/reoxygenation-induced lactate dehydrogenase (LDH) release by 90%. In conclusion, elevation of extracellular Mg2+ to 5 mM increased the fluorescence of the H2O2/NO-sensitive probe DCF without increasing that of the O2 −·-sensitive probe ETH, reduced Ca2+ accumulation, and decreased LDH release during reoxygenation of hypoxic cardiomyocytes. The reduction in LDH release, reflecting the protective effect of Mg2+, may be linked to the effect of Mg2+ on Ca2+ accumulation and/or ROS levels.

Differential responses of hydrogen peroxide, lipid peroxidation and antioxidant enzymes in Azolla microphylla exposed to paraquat and nitric oxide

Biologia ◽  
2012 ◽  
Vol 67 (6) ◽  
Author(s):  
Anjuli Sood ◽  
Charu Kalra ◽  
Sunil Pabbi ◽  
Prem Uniyal
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Antioxidative Enzymes ◽  
Guaiacol Peroxidase ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Concentration Dependent Manner ◽  
No Donor ◽  
Azolla Microphylla

AbstractThe present investigation was carried out to decipher the interplay between paraquat (PQ) and exogenously applied nitric oxide (NO) in Azolla microphylla. The addition of PQ (8 μM) increased the activities of superoxide dismutase (SOD), catalase (CAT), guaiacol peroxidase (GPX), ascorbate peroxidase (APX) by 1.7, 2.7, 3.9 and 1.9 folds respectively than that control in the fronds of Azolla. The amount of H2O2 was also enhanced by 2.7 times in the PQ treated plants than that of control. The supplementation of sodium nitroprusside (SNP) from 8–100 μM along with PQ, suppressed the activities of antioxidative enzymes and the amount of H2O2 compared to PQ alone. The drop in the activity of antioxidative enzymes — SOD, GPX, CAT and APX was highest (39.9%, 48.4%, 41.6% and 41.3% respectively) on the supplementation of 100 μM SNP with PQ treated fronds compared to PQ alone. The addition of NO scavengers along with NO donor in PQ treated fronds neutralized the effect of exogenously supplied NO. This indicates that NO can effectively protect Azolla against PQ toxicity by quenching reactive oxygen species. However, 200 μM of SNP reversed the protective effect of lower concentration of NO donor against herbicide toxicity. Our study clearly suggests that (i) SNP released NO can work both as cytoprotective and cytotoxic in concentration dependent manner and (ii) involvement of NO in protecting Azolla against PQ toxicity.

scholarly journals Effect of nitric oxide on exercise-induced proteinuria in rats

2003 ◽  
Vol 95 (5) ◽  
pp. 1867-1872 ◽  
Author(s):  
Filiz Gündüz ◽  
Oktay Kuru ◽  
Ümit Kemal Şentürk
Keyword(s):  
Nitric Oxide ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Mixed Type ◽  
Channel Blocker ◽  
Renal Hemodynamics ◽  
Urinary Protein ◽  
Exhaustive Exercise ◽  
No Donor ◽  
Protein Levels

Temporary proteinuria occurring after exercise is a common finding, and it is explained predominantly by alterations in renal hemodynamics. In this study, we investigated whether nitric oxide (NO), which is known to have an effect on renal hemodynamics and to increase during exercise, has a role in postexercise proteinuria. In the first step of this study, the effect of acute NO synthase blockage on exercise proteinuria was evaluated. The urinary protein levels in animals that performed acute exhaustive treadmill running exercise were considerably elevated compared with the control animals. Significantly elevated urinary protein levels were also detected in animals that received Nω-nitro-L-arginine methyl ester before exhaustion, compared with both control and exhausted groups, and mixed-type proteinuria was detected in electrophoresis, as in all exhausted animals. In the second step of the study, a NO donor (isosorbide mononitrate) was given to rats 1 h before exhaustive exercise. Mixed-type proteinuria and the elevation in urinary protein levels that occur as a consequence of exhaustive exercise were prevented by NO donor treatment. Finally, in the third step of our study, a calcium channel blocker (diltiazem), another vasodilator, was applied to the rats 1 h before exhaustive exercise. Urinary protein levels were not different in exhausted rats with or without calcium channel blocker treatment. On the other hand, in both groups, urinary protein levels were higher than in the control group. The tail-cuff blood pressure alterations caused by vasodilator drug applications before exercise were not different for NO donor and calcium channel blocker groups. These results suggest that endogenous NO might prevent the postexercise proteinuria from becoming more severe by affecting hemodynamic changes that occur during exercise.

scholarly journals Nitric oxide and cGMP protein kinase (cGK) regulate dendritic-cell migration toward the lymph-node–directing chemokine CCL19

Blood ◽  
2006 ◽  
Vol 107 (4) ◽  
pp. 1537-1545 ◽  
Author(s):  
Daniela Giordano ◽  
Dario M. Magaletti ◽  
Edward A. Clark
Keyword(s):  
Nitric Oxide ◽  
Cell Migration ◽  
Dendritic Cell ◽  
Focal Adhesions ◽  
Protective Effects ◽  
No Donor ◽  
Vasp Phosphorylation ◽  
Dendritic Cell Migration ◽  
Chemokine Ccl19

Dendritic-cell (DC) migration to secondary lymphoid organs is crucial for the initiation of adaptive immune responses. Although LPS up-regulates CCR7 on DCs, a second signal is required to enable them to migrate toward the chemokine CCL19 (MIP-3β). We found that the nitric oxide (NO) donor NOR4 provides a signal allowing LPS-stimulated DCs to migrate toward CCL19. NO affects DC migration through both the initial activation of the cGMP/cGMP kinase (cGMP/cGK) pathway and a long-term effect that reduced cGK activity via negative feedback. Indeed, migration of DCs toward CCL19, unlike migration toward CXCL12 (SDF-1α), required inhibition of cGK. LPS increased both cGK expression and cGK activity as measured by phosphorylation of the key cGK target vasodilator-stimulated phosphoprotein (VASP). Because cGK phosphorylation of VASP can disrupt focal adhesions and inhibit cell migration, LPS-induced VASP phosphorylation may prevent DCs from migrating without a second signal. Long-term NOR4 treatment inhibited the increase in cGK-dependent VASP phosphorylation, releasing this brake so that DCs can migrate. NO has been implicated in the regulation of autoimmunity through its effect on T cells. Our results suggest that NO regulation of DC migration and cytokine production may contribute to the protective effects of NO in autoimmune disorders.

scholarly journals Modulation of rat peripheral polymorphonuclear leukocyte response by nitric oxide and arginine

Blood ◽  
1994 ◽  
Vol 84 (8) ◽  
pp. 2741-2748 ◽  
Author(s):  
P Seth ◽  
R Kumari ◽  
M Dikshit ◽  
RC Srimal
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Methylene Blue ◽  
Polymorphonuclear Leukocytes ◽  
Reactive Oxygen Species Generation ◽  
Oxygen Species ◽  
Superoxide Generation ◽  
No Donor ◽  
Radical Generation ◽  
Leukocyte Response

The effect of nitric oxide (NO) on the luminol-dependent chemiluminescence (LCL) response of rat polymorphonuclear leukocytes (PMNLs) was analyzed by using sodium nitroprusside (SNP), a NO donor, and L-arginine (L-arg), a NO precursor. A significant reduction in the LCL intensity was observed in presence of SNP (100 mumol/L) or L-arg (5 or 10 mmol/L) in arachidonic acid (AA) phorbol ester (PMA) and formyl- methionyl-leucyl-phenylalanine stimulated PMNLs. However, opsonized zymosan-induced LCL was not attenuated significantly. Reduction in hydroxyl radical and superoxide generation was also observed in SNP- or L-arg-pretreated cells. D-Arg (10 mmol/L) pretreatment did not inhibit PMNLs' LCL response. Furthermore, methylene blue (5 mumol/L) and L-NG- mono methyl-L-arginine (100 or 300 mumol/L) significantly attenuated the LCL response, as induced by various agonists. Cyclic GMP did not alter the reactive oxygen species generation from rat PMNLs. In addition, AA-induced release of myeloperoxidase, a marker of azurophilic granules, was found to be enhanced in L-arg- (10 mmol/L) pretreated PMNLs. The results suggest that NO inhibits free radical generation from rat PMNLs.

scholarly journals Reactive Nitrogen and Oxygen Species Ameliorate Experimental Cryptosporidiosis in the Neonatal BALB/c Mouse Model

1999 ◽  
Vol 67 (11) ◽  
pp. 5885-5891 ◽  
Author(s):  
Gordon J. Leitch ◽  
Qing He
Keyword(s):  
Nitric Oxide ◽  
Oral Administration ◽  
Reactive Oxygen ◽  
Protective Role ◽  
Proximal Colon ◽  
Fecal Excretion ◽  
Reactive Nitrogen ◽  
Oxygen Species ◽  
No Donor ◽  
Plasma Nitrite

ABSTRACT Four-day-old BALB/c mice were infected by the oral administration of 50,000 Cryptosporidium parvum oocysts, and the resulting infection was scored histologically and by counting colonic oocysts. Infection occurred in the ileum and proximal colon (but not duodenum and jejunum), peaked on days 14 to 18, and was cleared between days 24 and 30. Nitric oxide (NO) appeared to play a protective role in this model as evidenced by the facts that plasma nitrite and nitrate levels increased during the period of peak parasitosis; immunohistochemically detected inducible nitric oxide synthase (iNOS) was increased in the ileum and colon enterocytes of infected animals; the NOS inhibitor l-N-iminoethyl lysine orN-nitro-l-arginine methyl ester (L-NAME) decreased the elevated plasma nitrite and nitrate levels while exacerbating the infection and increasing oocyst shedding; administration of a NO donor,S-nitroso-N-penicillamine, reduced oocyst and infection scores; and neonatal iNOS knockout mice exhibited a slightly longer infection than control animals. The oral administration of oocysts to L-NAME-treated BALB/c mice, but not control animals, between 24 and 40 days old resulted in the fecal excretion of oocysts 1 week later. Administration of the antioxidant ascorbic acid also exacerbated the C. parvum infection, suggesting a protective role for reactive nitrogen and/or reactive oxygen compounds, while administration of the superoxide scavenger superoxide dismutase exacerbated the infection. Taken together these data suggest that both reactive nitrogen and reactive oxygen species play protective roles in experimental cryptosporidiosis.

l-Arginine-NO pathway and CNS oxygen toxicity

1998 ◽  
Vol 84 (5) ◽  
pp. 1633-1638 ◽  
Author(s):  
Noemi Bitterman ◽  
Haim Bitterman
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Latent Period ◽  
Specific Inhibitor ◽  
Oxygen Toxicity ◽  
Absolute Pressure ◽  
The Novel ◽  
No Donor ◽  
Oxide Synthase ◽  
Different Doses

The involvement of thel-arginine-nitric oxide (NO) pathway in the pathogenesis of hyperoxia-induced seizures was studied by using agents controlling NO levels. We selected two inhibitors of nitric oxide synthase, the systemic inhibitor N ω-nitro-l-arginine methyl ester (l-NAME) and the novel cerebral-specific inhibitor 7-nitroindazole, and two generators of NO, the NO donor S-nitroso- N-acetylpenicillamine and the physiological precursorl-arginine. Rats with chronic cortical electrodes were injected intraperitoneally with different doses of one of the agents or their vehicles before exposure to 0.5 MPa O2 and O2 with 5% CO2 at an absolute pressure of 0.5 MPa. The duration of the latent period until the onset of electrical discharges in the electroencephalogram was used as an index of central nervous system O2 toxicity. The two nitric oxide synthase inhibitorsl-NAME and 7-nitroindazole significantly prolonged the latent period to the onset of seizures on exposure to both hyperbaric O2 and to the hypercapnic-hyperoxic mixture. Pretreatment with the NO donor S-nitroso- N-acetylpenicillamine significantly shortened the latent period, whereasl-arginine, the physiological precursor of NO, significantly prolonged the latent period to onset of seizures. Our results suggest that thel-arginine-NO pathway is involved in the pathophysiology of hyperoxia-induced seizures via various regulating mechanisms.

Regulation of an inwardly rectifying K+ channel by nitric oxide in cultured human proximal tubule cells

2004 ◽  
Vol 287 (3) ◽  
pp. F411-F417 ◽  
Author(s):  
Kazuyoshi Nakamura ◽  
Junko Hirano ◽  
Manabu Kubokawa
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase ◽  
Low Dose ◽  
Specific Inhibitor ◽  
High Dose ◽  
Channel Activity ◽  
No Donor ◽  
Proximal Tubule Cells ◽  
Tubule Cells ◽  
Inwardly Rectifying

We investigated the effects of nitric oxide (NO) on activity of the inwardly rectifying K+ channel in cultured human proximal tubule cells, using the cell-attached mode of the patch-clamp technique. An inhibitor of NO synthases, Nω-nitro-l-arginine methyl ester (l-NAME; 100 μM), reduced channel activity, which was restored by an NO donor, sodium nitroprusside (SNP; 10 μM) or 8-bromo-cGMP (8-BrcGMP; 100 μM). However, SNP failed to activate the channel in the presence of an inhibitor of soluble guanylate cyclase, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (10 μM). Similarly, the SNP effect was abolished by a protein kinase G (PKG)-specific inhibitor, KT-5823 (1 μM), but not by a protein kinase A-specific inhibitor, KT-5720 (500 nM). Another NO donor, S-nitroso- N-acetyl-d,l-penicillamine (10 μM), mimicked the SNP-induced channel activation. In contrast to the stimulatory effect of SNP at a low dose (10 μM), a higher dose of SNP (1 mM) reduced channel activity, which was not restored by 8-BrcGMP. Recordings of membrane potential with the slow whole cell configuration demonstrated that l-NAME (100 μM) and the high dose of SNP (1 mM) depolarized the cell by 10.1 ± 2.6 and 9.2 ± 1.0 mV, respectively, whereas the low dose of SNP (10 μM) hyperpolarized it by 7.1 ± 0.7 mV. These results suggested that the endogenous NO would contribute to the maintenance of basal activity of this K+ channel and hence the potential formation via a cGMP/PKG-dependent mechanism, whereas a high dose of NO impaired channel activity independent of cGMP/PKG-mediated processes.

scholarly journals THE EFFECTS OF NITRIC OXIDE ON SOME ANTIOXIDANT ENZYME ACTIVITIES UNDER SALT STRESS IN SUNFLOWER PLANTS

2019 ◽  
Vol 18 (5) ◽  
pp. 171-179
Author(s):  
Fusun Yurekli ◽  
Oguz A. Kirecci ◽  
Ilknur Celik
Keyword(s):  
Nitric Oxide ◽  
Salt Stress ◽  
Antioxidant Enzyme ◽  
Enzyme Activities ◽  
Antioxidant Enzyme Activities ◽  
Oxygen Species ◽  
Negative Effects ◽  
No Donor ◽  
Tolerant Variety ◽  
Leaf Tissues

The effects of externally applied sodium nitroprusside on superoxide dismutase (SOD), glutathione peroxidase (GPx), ascorbate peroxidase (APX), and catalase (CAT) antioxidant enzyme activities, nitric oxide (NO) levels have investigated in salt stress resistant and sensitive sunflower plants. NaCl treatments and SNP treatments simultaneous with salt application (NaCl + SNP) were performed. SOD, GPx, APX and CAT antioxidant enzyme activities and NO levels, showed differences in leaf tissues treated with 100 µM SNP, different concentrations of NaCl, and NaCl + SNP. SOD, GPx and APX enzyme activities were generally increased in sensitive variety but decreased in tolerant variety. However, while generally increase in CAT enzyme activity was determined in tolerant type, a reduction was established in sensitive type. An increase was determined in both types in NO levels. It is evident from these results that administration of NO donor SNP can cope with reactive oxygen species in both varieties. This study indicates that the negative effects of salt stress on different sun flower varieties can be recovered by nitric oxide.

Nitric-oxide-dependent activation of pig oocytes: the role of the cGMP-signalling pathway

Zygote ◽  
2006 ◽  
Vol 14 (1) ◽  
pp. 9-16 ◽  
Author(s):  
J. Petr ◽  
R. Rajmon ◽  
E. Chmelíková ◽  
M. Tománek ◽  
V. Lánská ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Guanylyl Cyclase ◽  
Specific Inhibitor ◽  
Calcium Ionophore ◽  
Signalling Pathway ◽  
Nitric Oxide Donor ◽  
Ionophore A23187 ◽  
Dependent Manner ◽  
Oocyte Activation ◽  
No Donor

Pig oocytes matured in vitro were parthenogenetically activated (78%) after treatment with 2 mM nitric oxide-donor (±)-S-nitroso-N-acetylpenicillamine (SNAP) for 24 h. Inhibition of soluble guanylyl cyclase with the specific inhibitors 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) or 6-anilino-5,8-quinolinequinone (LY83583) suppressed the SNAP-induced activation in a dose-dependent manner (23% of activated oocytes after treatment with 400 μM ODQ; 12% of activated oocytes after treatment with 40 μM LY83583). 8-Bromo-cyclic guanosine monophosphate (8-Br-cGMP), a phosphodiesterase-resistant analogue of cGMP, enhances the effect of suboptimal doses (0.1 or 0.5 mM) of the NO donor SNAP. DT3, a specific inhibitor of cGMP-dependent protein kinase (PKG, PKG), is also able to inhibit the activation of pig oocytes after NO donor treatment. Involvement of the cGMP-dependent signalling pathway is specific for NO-induced oocyte activation, because both the guanylyl cyclase inhibitor ODQ and the PKG inhibitor DT3 are unable to inhibit activation in oocytes treated with the calcium ionophore A23187. These data indicate that the activation of pig oocytes with an NO donor is cGMP-dependent and that PKG plays an important role in this mode of oocyte activation.

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