Sodium Nitroprussidenitric oxide (NO) donor CAS# 14402-89-2 |
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Quality Control & MSDS
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Chemical structure
3D structure
| Cas No. | 14402-89-2 | SDF | Download SDF |
| PubChem ID | 11963579 | Appearance | Powder |
| Formula | C5FeN6Na2O | M.Wt | 261.92 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | Ro 21-2498 | ||
| Solubility | H2O : ≥ 100 mg/mL (381.80 mM) DMSO : 33.33 mg/mL (127.25 mM; Need ultrasonic) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | disodium;iron(4+);nitroxyl anion;pentacyanide | ||
| SMILES | [C-]#N.[C-]#N.[C-]#N.[C-]#N.[C-]#N.[N-]=O.[Na+].[Na+].[Fe+4] | ||
| Standard InChIKey | PECOKVKJVPMJBN-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/5CN.Fe.NO.2Na/c5*1-2;;1-2;;/q5*-1;+4;-1;2*+1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Sodium Nitroprusside is a potent vasodilator working through releasing NO spontaneously in blood.
Target: Others
Sodium Nitroprusside is a potent vasodilator. Sodium nitroprusside has potent vasodilating effects in arterioles and venules. Sodium Nitroprusside breaks down in circulation to release nitric oxide (NO). NO activates guanylate cyclase in vascular smooth muscle and increases intracellular production of cGMP. The end result is vascular smooth muscle relaxation, which allow vessels to dilate [1]. Sodium nitroprusside decreases the proliferation of vascular smooth muscle cells [2]. Sodium nitroprusside (5 mg/kg) significantly reduces the intestinal ischemiareperfusion injury as a nitric oxide donor in rats [3]. References: | |||||
Sodium Nitroprusside Dilution Calculator
Sodium Nitroprusside Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.818 mL | 19.0898 mL | 38.1796 mL | 76.3592 mL | 95.449 mL |
| 5 mM | 0.7636 mL | 3.818 mL | 7.6359 mL | 15.2718 mL | 19.0898 mL |
| 10 mM | 0.3818 mL | 1.909 mL | 3.818 mL | 7.6359 mL | 9.5449 mL |
| 50 mM | 0.0764 mL | 0.3818 mL | 0.7636 mL | 1.5272 mL | 1.909 mL |
| 100 mM | 0.0382 mL | 0.1909 mL | 0.3818 mL | 0.7636 mL | 0.9545 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Sodium Nitroprusside is a potent nitric oxide (NO) donor.
NO is an important cellular signaling molecule and a powerful vasodilator in the blood, thus resulting in vasodilation and increasing blood flow.
Sodium nitroprusside is a potent nitric oxide (NO) donor by releasing NO into blood. Sodium nitroprusside inhibited the contractile response of Ca2+-depleted depolarized rat aorta to extra-cellular Ca2+ and Ca2+ uptake induced by K+. Also, sodium nitroprusside decreased the rapid contraction phase induced by noradrenaline [1]. In isolated bull veins, sodium nitroprusside relaxed bull veins contraction induced by noradrenaline in a dose-dependent way [2]. In platelet-rich plasmas (PRP), sodium nitroprusside significantly inhibited platelets aggregation and also inhibited ADP and ATP release from platelets induced by collagen, which might be due to contraction of platelet smooth muscle-like protein [3].
In patients with total hip replacement under anesthesia, sodium nitroprusside (100 μg/ml) induced hypotension and reduced surgical blood loss [4].
References:
[1]. Kreye VA, Baron GD, Lüth JB, et al. Mode of action of sodium nitroprusside on vascular smooth muscle. Naunyn Schmiedebergs Arch Pharmacol, 1975, 288(4): 381-402.
[2]. Gmeiner R, Riedl J, Baumgartner H. Effect of sodium nitroprusside on myocardial performance and venous tone. Eur J Pharmacol, 1975, 31(2): 287-291.
[3]. Saxon A, Kattlove HE. Platelet inhibition by sodium nitroprusside, a smooth muscle inhibitor. Blood, 1976, 47(6): 957-961.
[4]. Lawson NW, Thompson DS, Nelson CL, et al. A dosage nomogram for sodium nitroprusside-induced hypotension under anesthesia. Anesth Analg, 1976, 55(4): 574-580.
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Mitigation by sodium nitroprusside of the effects of salinity on the morpho-physiological and biochemical characteristics of Rubus idaeus under in vitro conditions.[Pubmed:28250585]
Physiol Mol Biol Plants. 2017 Jan;23(1):73-83.
This study examined the changes brought about by Sodium Nitroprusside (SNP) in the effects of salinity on the morpho-physiological and biochemical characteristics of Rubus idaeus var. Danehdrosht. Raspberry shoot-tip explants were cultured on Murashige and Skoog medium supplemented with a growth regulator that combined benzyleadenine (1 mg/l), indol-3-butyric acetic acid (0.2 mg/l), SNP (0, 50 and 100 microM) and sodium chloride (0, 50 and 100 mM). The results showed that salinity stress significantly decreased morpho-physiological and biochemical characteristics such as RWC, MSI and total protein content in regenerated explants and significantly increased the total soluble sugar, proline contents, peroxidase and superoxide dismutase activity in compared to the control. However, SNP treatments mitigated the impacts of salinity on morphological and physiological characteristics in raspberry shoot-tip explants by increasing the accumulation of proline content, total protein content and total soluble sugar in line with increasing antioxidant enzyme activity under salinity conditions.
Mechanisms underlying sodium nitroprusside-induced tolerance in the mouse aorta: Role of ROS and cyclooxygenase-derived prostanoids.[Pubmed:28341178]
Life Sci. 2017 May 1;176:26-34.
AIMS: To determine the role of reactive oxygen species (ROS) on Sodium Nitroprusside (SNP)-induced tolerance. Additionally, we evaluated the role of ROS on NF-kappaB activation and pro-inflammatory cytokines production during SNP-induced tolerance. MAIN METHODS: To induce in vitro tolerance, endothelium-intact or -denuded aortic rings isolated from male Balb-c mice were incubated for 15, 30, 45 or 60min with SNP (10nmol/L). KEY FINDINGS: Tolerance to SNP was observed after incubation of endothelium-denuded, but not endothelium-intact aortas for 60min with this inorganic nitrate. Pre-incubation of denuded rings with tiron (superoxide anion (O2(-)) scavenger), and the NADPH oxidase inhibitors apocynin and atorvastatin reversed SNP-induced tolerance. l-NAME (non-selective NOS inhibitor) and l-arginine (NOS substrate) also prevented SNP-induced tolerance. Similarly, ibuprofen (non-selective cyclooxygenase (COX) inhibitor), nimesulide (selective COX-2 inhibitor), AH6809 (prostaglandin PGF2alpha receptor antagonist) or SQ29584 [PGH2/thromboxane TXA2 receptor antagonist] reversed SNP-induced tolerance. Increased ROS generation was detected in tolerant arteries and both tiron and atorvastatin reversed this response. Tiron prevented tolerance-induced increase on O2(-) and hydrogen peroxide (H2O2) levels. The increase onp65/NF-kappaB expression and TNF-alpha production in tolerant arteries was prevented by tiron. The major new finding of our study is that SNP-induced tolerance is mediated by NADPH-oxidase derived ROS and vasoconstrictor prostanoids derived from COX-2, which are capable of reducing the vasorelaxation induced by SNP. Additionally, we found that ROS mediate the activation of NF-kappaB and the production of TNF-alpha in tolerant arteries. SIGNIFICANCE: These findings identify putative molecular mechanisms whereby SNP induces tolerance in the vasculature.
Sodium Nitroprusside Changed The Metabolism of Mesenchymal Stem Cells to An Anaerobic State while Viability and Proliferation Remained Intact.[Pubmed:28367425]
Cell J. 2017 Apr-Jun;19(1):146-158. Epub 2016 Dec 21.
OBJECTIVE: We used Sodium Nitroprusside (SNP), a nitric oxide (NO) releasing molecule, to understand its effect on viability and proliferation of rat bone marrow mesenchymal stem cells (BM-MSCs). MATERIALS AND METHODS: This experimental study evaluated the viability and morphology of MSCs in the presence of SNP (100 to 2000 microM) at 1, 5, and 15 hours. We chose the 100, 1000, and 2000 microM concentrations of SNP for one hour exposure for further analyses. Cell proliferation was investigated by the colony forming assay and population doubling number (PDN). Na(+), K(+), and Ca(2+) levels as well as activities of lactate dehydrogenase (LDH), alkaline phosphatase (ALP), aspartate transaminase (AST), and alanine transaminase (ALT) were measured. RESULTS: The viability of MSCs dose-dependently reduced from 750 microM at one hour and 250 microM at 5 and 15 hours. The 100 microM caused no change in viability, however we observed a reduction in the cytoplasmic area at 5 and 15 hours. This change was not observed at one hour. The one hour treatment with 100 microM of SNP reduced the mean colony numbers but not the diameter when the cells were incubated for 7 and 14 days. In addition, one hour treatment with 100 microM of SNP significantly reduced ALT, AST, and ALP activities whereas the activity of LDH increased when incubated for 24 hours. The same treatment caused an increase in Ca(2+) and reduction in Na(+) content. The 1000 and 2000 microM concentrations reduced all the factors except Ca(2+) and LDH which increased. CONCLUSION: The high dose of SNP, even for a short time, was toxic. The low dose was safe with respect to viability and proliferation, especially over a short time. However elevated LDH activity might increase anaerobic metabolism.
Similar effect of sodium nitroprusside and acetylsalicylic acid on antioxidant system improvement in mouse liver but not in the brain.[Pubmed:28232079]
Biochimie. 2017 Apr;135:181-185.
BACKGROUND: The aim of the present study was to analyze the relative antioxidant effects of acetylsalicylic acid (ASA) and Sodium Nitroprusside (SNP) in mouse liver and brain. METHODS: The activity of rhodanese, 3-mercaptopyruvate sulfurtransferase (MPST) and gamma-cystathionase (CSE), functioning as antioxidant proteins and capable of producing H2S, was investigated in mouse liver and brain after intraperitoneal once a day administration of Sodium Nitroprusside (5 mg/kg body weight) or acetylsalicylic acid (500 mg/kg body weight) continued for 5 days. The tissues were homogenized and then the obtained supernatants were used for further determinations. At the same time, the levels of sulfane sulfur, reduced and oxidized glutathione, cysteine, cystine, and cystathionine were also studied in these tissues. RESULTS: Both ASA and SNP show a statistically significant increase of sulfurtransferases activities in liver. The mechanism of action of Sodium Nitroprusside appears to consist in liberation of nitric oxide (NO), an important signaling molecule in the mammalian body. SNP also releases cyanide ions, which are converted in the liver to thiocyanate by the enzyme rhodanese and/or MPST and/or gamma-cystathionase - the activities of all the enzymes were elevated in reaction to SNP. The action of gamma-cystathionase is dependent upon converting cystathionine to cysteine, a precursor of the major cellular antioxidant, glutathione. Under oxidizing conditions, an increase in cystathionine beta-synthase activity might indirectly result in an increase in the antioxidant glutathione level; this was reflected by the increased GSH/GSSG ratio in the liver, but not in the brain, where a trace activity of gamma-cystathionase is normally detected. CONCLUSION: The results of the present investigations show that ASA and SNP may stimulate the GSH-dependent antioxidant system and protect liver cells from oxidative stress. An increased activity of the H2S-producing enzymes and the increased GSH/GSSG ratio may lead to an elevated level of H2S, a molecule with antioxidant properties. A similar effect was not observed in the brain. In case of both Sodium Nitroprusside and aspirin administration, homeostasis of sulfane sulfur level was noted in both the liver and brain.
