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S0501

Sigma-Aldrich

Sodium nitroprusside dihydrate

Synonym(s):

Nitroprusside sodium, SNP, Sodium nitroferricyanide, Sodium pentacyanonitrosylferrate

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About This Item

Linear Formula:
Na2[Fe(CN)5NO] · 2H2O
CAS Number:
Molecular Weight:
297.95
EC Number:
MDL number:
UNSPSC Code:
12352300

SMILES string

O.O.[Na+].[Na+].O=N[Fe--](C#N)(C#N)(C#N)(C#N)C#N

InChI

1S/5CN.Fe.NO.2Na.2H2O/c5*1-2;;1-2;;;;/h;;;;;;;;;2*1H2/q;;;;;2*-1;2*+1;;

InChI key

OIRZWVYIQXBRFC-UHFFFAOYSA-N

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Biochem/physiol Actions

Releases NO in vivo, thus activating guanylyl cyclase, ADP-ribosyltransferase, and cyclooxygenase and inhibiting lipoxygenase. Induces vasodilation and inhibits platelet aggregation.

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Skull and crossbones

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Danger

hcodes

Hazard Classifications

Acute Tox. 3 Oral

Storage Class

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Faceshields, Gloves, type P2 (EN 143) respirator cartridges


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Feelisch, M.
Journal of Cardiovascular Pharmacology, 17, S25-S25 (1991)
B Brüne et al.
The Journal of biological chemistry, 264(15), 8455-8458 (1989-05-25)
Sodium nitroprusside is a vasodilator and an inhibitor of platelet activation. It is thought that these effects are mediated by the spontaneous release of nitric oxide and stimulation of cytosolic guanylate cyclase. We have found that sodium nitroprusside (5-200 microM)
C M Roos et al.
Journal of applied physiology (Bethesda, Md. : 1985), 77(1), 51-57 (1994-07-01)
We localized the sites of vasodilation of inhaled nitric oxide (NO), a selective pulmonary vasodilator, and sodium nitroprusside (SNP) in isolated rat lungs. The sites were determined by analyzing the arterial, venous, and double-occlusion data with a two-resistor (small arteries
F J Azula et al.
Molecular pharmacology, 50(2), 367-379 (1996-08-01)
Different drugs that elevate the cGMP levels inhibit the agonist-induced platelet activation. The mechanisms of action of cGMP probably include inhibition of both phospholipase C and the increase in intracellular Ca2+ concentration, and these effects seem to be mediated by
D Salvemini et al.
The Journal of clinical investigation, 97(11), 2562-2568 (1996-06-01)
We have evaluated the contributions of nitric oxide (NO) and prostacyclin (PGI2) in the in vivo antiplatelet effects of clinically useful nitrovasodilators. In rats, intravenous infusion of three NO donors, glyceryl trinitrate, sodium nitroprusside, or 3'-morpholinosydnonimine, the stable metabolite of

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