Acute and repeated exposure with the nitric oxide (NO) donor sodium nitroprusside (SNP) differentially modulate responses in a rat model of anxiety

Nitric Oxide ◽  
2017 ◽  
Vol 69 ◽  
pp. 56-60 ◽  
Author(s):  
Martha A. Orfanidou ◽  
Anastasios Lafioniatis ◽  
Aikaterini Trevlopoulou ◽  
Ntilara Touzlatzi ◽  
Nikolaos Pitsikas
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Rat Model ◽  
Repeated Exposure ◽  
No Donor

Nitric oxide increases fluid extravasation from the splenic circulation of the rat

2001 ◽  
Vol 280 (4) ◽  
pp. R959-R967 ◽  
Author(s):  
Peter S. Andrew ◽  
Yiming Deng ◽  
Richard Sultanian ◽  
Susan Kaufman
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Lymphatic System ◽  
Resistance Arteries ◽  
No Donor ◽  
Fluid Extravasation ◽  
Resistance Vessels ◽  
Blood Inflow ◽  
The Difference ◽  
Arteries And Veins

We hypothesized that nitric oxide (NO) contributes to intrasplenic fluid extravasation by inducing greater relaxation in splenic resistance arteries than veins such that intrasplenic microvascular pressure (PC) rises. Fluid efflux was estimated by measuring the difference between splenic blood inflow and outflow. Intrasplenic infusion of the NO donor S-nitroso- N-acetylpenicillamine (SNAP) (0.3 μg · 10 μl−1 · min−1) caused a significant increase in intrasplenic fluid efflux (baseline: 0.8 ± 0.4 ml/min, n = 10 vs. peak rise during SNAP infusion: 1.3 ± 0.4 ml/min, n = 10; P < 0.05). Intrasplenic PC was measured in the isolated, blood-perfused rat spleen. Intrasplenic infusion of SNAP (0.1 μg · 10 μl−1 · min−1) caused a significant increase in PC (saline: 10.9 ± 0.2 mmHg, n = 3 vs. SNAP: 12.2 ± 0.2 mmHg, n = 3; P < 0.05). Vasoreactivity of preconstricted splenic resistance vessels to sodium nitroprusside (SNP) (1 × 10−12-1 × 10−4 M) and SNAP (1 × 10−10-3 × 10−4 M) was investigated with the use of a wire myograph system. Significantly greater relaxation of arterioles than of venules occurred with both SNP (%maximal vasorelaxation: artery 96 ± 2.3, n = 9 vs. vein 26 ± 1.9, n = 10) and SNAP (%maximal vasorelaxation: artery 50 ± 3.5, n = 11 vs. vein 32 ± 1.7, n = 8). These results are consistent with our proposal that differential vasoreactivity of splenic resistance arteries and veins to NO elevates intrasplenic PC and increases fluid extravasation into the systemic lymphatic system.

scholarly journals Sodium nitroprusside prevents the detrimental effects of glucose on the neurovascular unit and behaviour in zebrafish

2019 ◽  
Author(s):  
K. Chhabria ◽  
A. Vouros ◽  
C. Gray ◽  
R.B. MacDonald ◽  
Z. Jiang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Optic Tectum ◽  
Neurovascular Unit ◽  
Cell Number ◽  
Neuronal Activation ◽  
Negative Effects ◽  
Mural Cell ◽  
No Donor ◽  
Glucose Exposure

AbstractDiabetes is associated with dysfunction of the neurovascular unit, although the mechanisms of this are incompletely understood, and currently no treatment exists to prevent these negative effects. We previously found that the NO donor sodium nitroprusside (SNP) prevents the detrimental effect of glucose on neurovascular coupling in zebrafish. We therefore sought to establish the wider effects of glucose exposure on both the neurovascular unit and on behaviour in zebrafish and the ability of SNP to prevent these.We incubated 4 days post fertilisation (dpf) zebrafish embryos in 20mM glucose or mannitol for five days until 9dpf, with or without 0.1mM SNP co-treatment for 24h (8-9dpf), and quantified vascular nitric oxide reactivity, vascular mural cell number, expression of aklf2areporter, glial fibrillary acidic protein (GFAP) and TRPV4, as well as spontaneous neuronal activation at 9dpf, all in the optic tectum. We also assessed the effect on light/dark preference and locomotory characteristics during free-swimming studies.We find that glucose exposure significantly reduced nitric oxide reactivity,klf2areporter expression, vascular mural cell number and TRPV4 expression, while significantly increasing spontaneous neuronal activation and GFAP expression (all in the optic tectum). Furthermore, when we examined larval behaviour we found glucose exposure significantly altered light/dark preference and high and low speed locomotion while in light. Co-treatment with SNP reversed all these molecular and behavioural effects of glucose exposure.Our findings comprehensively describe the negative effects of glucose exposure on the vascular anatomy, molecular phenotype, and function of the optic tectum and on whole organism behaviour. We also show that SNP or other NO donors may represent a therapeutic strategy to ameliorate the complications of diabetes on the neurovascular unit.

scholarly journals Polyamine Induction in Postharvest Banana Fruits in Response to NO Donor SNP Occurs via l-Arginine Mediated Pathway and Not via Competitive Diversion of S-Adenosyl-l-Methionine

Antioxidants ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 358 ◽  
Author(s):  
Veeresh Lokesh ◽  
Girigowda Manjunatha ◽  
Namratha S. Hegde ◽  
Mallesham Bulle ◽  
Bijesh Puthusseri ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Arginine Decarboxylase ◽  
No Donor ◽  
Expression Studies ◽  
Common Precursor ◽  
Competitive Action ◽  
Gene Expression Studies

Nitric oxide (NO) is known to antagonize ethylene by various mechanisms; one of such mechanisms is reducing ethylene levels by competitive action on S-adenosyl-L-methionine (SAM)—a common precursor for both ethylene and polyamines (PAs) biosynthesis. In order to investigate whether this mechanism of SAM pool diversion by NO occur towards PAs biosynthesis in banana, we studied the effect of NO on alterations in the levels of PAs, which in turn modulate ethylene levels during ripening. In response to NO donor sodium nitroprusside (SNP) treatment, all three major PAs viz. putrescine, spermidine and spermine were induced in control as well as ethylene pre-treated banana fruits. However, the gene expression studies in two popular banana varieties of diverse genomes, Nanjanagudu rasabale (NR; AAB genome) and Cavendish (CAV; AAA genome) revealed the downregulation of SAM decarboxylase, an intermediate gene involved in ethylene and PA pathway after the fifth day of NO donor SNP treatment, suggesting that ethylene and PA pathways do not compete for SAM. Interestingly, arginine decarboxylase belonging to arginine-mediated route of PA biosynthesis was upregulated several folds in response to the SNP treatment. These observations revealed that NO induces PAs via l-arginine-mediated route and not via diversion of SAM pool.

scholarly journals The Nitric Oxide (NO) Donor Sodium Nitroprusside (SNP) and Its Potential for the Schizophrenia Therapy: Lights and Shadows

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3196
Author(s):  
Elli Zoupa ◽  
Nikolaos Pitsikas
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Cognitive Deficits ◽  
Negative Symptoms ◽  
Mental Disease ◽  
No Production ◽  
No Donor ◽  
No Donors ◽  
Worldwide Population ◽  
The Brain

Schizophrenia is a severe psychiatric disorder affecting up to 1% of the worldwide population. Available therapy presents different limits comprising lack of efficiency in attenuating negative symptoms and cognitive deficits, typical features of schizophrenia and severe side effects. There is pressing requirement, therefore, to develop novel neuroleptics with higher efficacy and safety. Nitric oxide (NO), an intra- and inter-cellular messenger in the brain, appears to be implicated in the pathogenesis of schizophrenia. In particular, underproduction of this gaseous molecule is associated to this mental disease. The latter suggests that increment of nitrergic activity might be of utility for the medication of schizophrenia. Based on the above, molecules able to enhance NO production, as are NO donors, might represent a class of compounds candidates. Sodium nitroprusside (SNP) is a NO donor and is proposed as a promising novel compound for the treatment of schizophrenia. In the present review, we intended to critically assess advances in research of SNP for the therapy of schizophrenia and discuss its potential superiority over currently used neuroleptics.

scholarly journals Nitric Oxide Ameliorates Plant Metal Toxicity by Increasing Antioxidant Capacity and Reducing Pb and Cd Translocation

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1981
Author(s):  
Abolghassem Emamverdian ◽  
Yulong Ding ◽  
James Barker ◽  
Farzad Mokhberdoran ◽  
Muthusamy Ramakrishnan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heavy Metal ◽  
Sodium Nitroprusside ◽  
Metal Toxicity ◽  
Heavy Metal Toxicity ◽  
No Synthase ◽  
Bamboo Species ◽  
No Donor ◽  
Cd Toxicity ◽  
Synthase Inhibitor

Recently, nitric oxide (NO) has been reported to increase plant resistance to heavy metal stress. In this regard, an in vitro tissue culture experiment was conducted to evaluate the role of the NO donor sodium nitroprusside (SNP) in the alleviation of heavy metal toxicity in a bamboo species (Arundinaria pygmaea) under lead (Pb) and cadmium (Cd) toxicity. The treatment included 200 µmol of heavy metals (Pb and Cd) alone and in combination with 200 µM SNP: NO donor, 0.1% Hb, bovine hemoglobin (NO scavenger), and 50 µM L-NAME, N(G)-nitro-L-arginine methyl ester (NO synthase inhibitor) in four replications in comparison to controls. The results demonstrated that the addition of L-NAME and Hb as an NO synthase inhibitor and NO scavenger significantly increased oxidative stress and injured the cell membrane of the bamboo species. The addition of sodium nitroprusside (SNP) for NO synthesis increased antioxidant activity, protein content, photosynthetic properties, plant biomass, and plant growth under heavy metal (Pb and Cd) toxicity. It was concluded that NO can increase plant tolerance for metal toxicity with some key mechanisms, such as increasing antioxidant activities, limiting metal translocation from roots to shoots, and diminishing metal accumulation in the roots, shoots, and stems of bamboo species under heavy metal toxicity (Pb and Cd).

The role of nitric oxide in the regulation of the electrical activity of the trigeminal nerve in the rat

2021 ◽  
Author(s):  
S.O. Svitko ◽  
K.S. Koroleva ◽  
G.F. Sitdikova ◽  
K.A. Petrova
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Trigeminal Nerve ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
No Synthase ◽  
The Body ◽  
No Donor ◽  
No Signaling

Nitric oxide (NO) is a gaseous signaling molecule that regulates a number of physiological functions, including its role in the formation of migraine has been established. NO is endogenously produced in the body from L-arginine by NO synthase. The NO donor, nitroglycerin, is a trigger of migraine in humans and is widely used in the modeling of this disease in animals, which suggests the involvement of components of the NO signaling cascade in the pathogenesis of migraine. Based on the results obtained, it was found that an increase in the concentration of both the substrate for the synthesis of NO, L-arginine, and the NO donor, sodium nitroprusside, has a pro-nociceptive effect in the afferents of the trigeminal nerve. In this case, the effect of sodium nitroprusside is associated with the activation of intracellular soluble guanylate cyclase. Key words: nitric oxide, migraine, trigeminal nerve, L-arginine, guanylate cyclase, sodium nitroprusside, nociception.

The Role of Nitric Oxide in Regulation of Red Blood Cell Deformability.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3730-3730
Author(s):  
Xiaojun He ◽  
Ivan Azarov ◽  
Beth Gordon ◽  
Daniel B. Kim-Shapiro ◽  
Samir K. Ballas
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Electron Paramagnetic Resonance Spectroscopy ◽  
Flow Channel ◽  
Resonance Spectroscopy ◽  
No Production ◽  
Cell Deformability ◽  
No Donor ◽  
Physiol Heart Circ ◽  
Rbc Deformability

Abstract Nitric Oxide (NO) has been suggested to modulate the deformability of red blood cells (RBCs). Bor-Kucukatay (Bor-Kucukatay et al. Am J Physiol Heart Circ Physiol284: H1577, 2003) found that cells incubated with 1 μM of the NO donor sodium nitroprusside lead to a small but significant increase RBC deformability as measured by ektacytometry. However, no significant effect was seen at lower or higher concentrations of sodium nitroprusside or for any concentration of another NO donor, diethylenetriamine NONOate. Kleinbongard (Kleinbongard et al. Blood10; 3992, 2005) found large increases in red cell deformability as a function of added arginine (the substrate for Nitric Oxide Synthase) by measuring the flow rate through filters. On the other hand, using cell aspiration techniques, Bateman (Bateman et al. Am J Physiol Heart Circ Physiol 280; H2848 H2001) found that NO production during sepsis causes a decrease in RBC deformability. Clearly more work is needed to determine the effects of NO on RBC deformability. The present work was undertaken to further investigate the effect of NO on normal and sickle RBC deformability. ProLi NONOate, arginine, and nitrite (which can be reduced to NO by hemoglobin (Hb), were incubated with blood at various concentrations over a period of 2 hours. Nitrosyl Hb and MetHb formed due to the interaction between NO and RBCs were quantified by electron paramagnetic resonance spectroscopy. The deformability was measured using a flow channel laser diffraction similar to ektacytometry (Huang et al. Am J Hematol67; 151, 2001, Biophys J85; 2374, 2003) with a stress range from 0 to 1,000 Pa. Diffraction patterns produced by deformed cells were analyzed by Matlab®. The deformability coefficients were compared to the control (n=6 per experiment condition). Our results suggested that ProLi NONOate did not significantly effect the deformability of normal RBCs. In a single case, ProLi NONOate improved the deformability of poorly deformable sickle red cells and this result is being studied further. Using our flow channel assay, we did not find any significant affects of arginine on RBC deformability. In addition, our studies involving nitrite, performed under both oxygenated and deoxygenated conditions, suggested that nitrite has no significant effect on RBC deformability. In summary, NO didn’t significantly affect the deformability of normal RBCs, and its potential effects on sickle RBCs needs to be further investigated.

Nitric oxide: role in venular permeability recovery after histamine challenge

1999 ◽  
Vol 277 (5) ◽  
pp. H2010-H2016 ◽  
Author(s):  
Hamda Al-Naemi ◽  
Ann L. Baldwin
Keyword(s):  
Nitric Oxide ◽  
Mast Cells ◽  
Sodium Nitroprusside ◽  
Blood Vessels ◽  
Inflammatory Mediator ◽  
Subsequent Treatment ◽  
The Other ◽  
Epifluorescence Microscopy ◽  
No Donor ◽  
Histamine Challenge

Histamine is an inflammatory mediator produced by mast cells that reside close to blood vessels. It causes a transient increase in venular permeability and stimulates endothelial production of nitric oxide (NO). In this study, we investigated the role that NO plays in the permeability recovery and evaluated the response of mast cells. The mesenteric microvasculature of anesthetized rats was suffused with 10−3 M histamine for 3 min and then perfused with the NO donor sodium nitroprusside (SNP; 10−6 M), the NO inhibitor N G-monomethyl-l-arginine (l-NMMA; 10−5 M), its enantiomer (d-NMMA; 10−5 M), or HEPES-buffered saline containing 0.5% BSA for 15 min. This was replaced by FITC-albumin for 3 min, followed by fixative. The vasculature was visualized using epifluorescence microscopy and was stained for mast cells. Preparations treated with histamine only showed discrete FITC-albumin leaks. Subsequent inhibition of NO increased venular FITC-albumin leaks and prevented permeability recovery, whereas subsequent treatment with SNP decreased the histamine-induced venular leaks. Mast cells degranulated due to histamine and the other treatment combinations. In conclusion, inhibition of NO prevented permeability recovery and depleted mast cells of their histamine content.

scholarly journals Sodium nitroprusside, a nitric oxide donor, fails to bypass the block of neuronal differentiation in PC12 cells imposed by a dominant negative Ras protein

2012 ◽  
Vol 17 (3) ◽  
Author(s):  
Judit Bátor ◽  
Judit Varga ◽  
Gergely Berta ◽  
Tamar Barbakadze ◽  
David Mikeladze ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Neuronal Differentiation ◽  
Pc12 Cells ◽  
P53 Protein ◽  
Dominant Negative ◽  
Nitric Oxide Donor ◽  
Dominant Negative Mutant ◽  
No Donor ◽  
Ras Protein

AbstractNitric oxide (NO) is a mediator of a diverse array of inter- and intracellular signal transduction processes. The aim of the present study was to analyze its possible role as a second messenger in the process of neuronal differentiation of PC12 pheochromocytoma cells. Upon NGF treatment wildtype PC12 cells stop dividing and develop neurites. In contrast, a PC12 subclone (designated M-M17-26) expressing a dominant-negative mutant Ras protein keeps proliferating and fails to grow neurites after NGF treatment. Sodium nitroprusside (SNP), an NO donor, was found to induce the p53 protein and to inhibit proliferation of both PC12 and M-M17-26 cells, but failed to induce neuronal differentiation in these cell lines. Key signaling pathways (the ERK and Akt pathways) were also not affected by SNP treatment, and the phosphorylation of CREB transcription factor was only slightly stimulated. It is thus concluded from the results presented in this paper that NO is unable to activate signaling proteins acting downstream or independent of Ras that are required for neuronal differentiation.

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