Sodium nitroprusside

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Sodium nitroprusside
Idealized depiction of this compound (top), and a picture of a sample (bottom).
Systematic (IUPAC) name
disodium pentacyano(nitroso)irondiuide
Clinical data
Trade names Nipride, Nitropress
AHFS/ Monograph
License data
  • AU: C
  • US: C (Risk not ruled out)
Routes of
Legal status
Legal status
Pharmacokinetic data
Bioavailability 100% (Intravenous)
Metabolism By haemoglobin being converted to cyanmethaemoglobin and cyanide ions
Biological half-life <2 minutes (3 days for thiocyanate metabolite)
Excretion Renal (100%; as thiocyanate)[1]
CAS Number 13755-38-9
ATC code C02DD01 (WHO)
PubChem CID 11953895
DrugBank DB00325
ChemSpider 21170789
Synonyms SNP
Chemical data
Formula C5FeN6Na2O
Molar mass 261.918
Physical data
Density 1.72 g/cm3
Solubility in water 100 mg/mL (20 °C)

Sodium nitroprusside is an inorganic compound with the formula Na2[Fe(CN)5NO], usually encountered as the dihydrate, Na2[Fe(CN)5NO]·2H2O.[2] This red-colored sodium salt dissolves in water ethanol to give solutions containing the free complex dianion [Fe(CN)5NO]2−.

This compound is used as a drug. In this role it is abbreviated SNP, and it has tradenames like Nitropress. It acts as a drug by releasing nitric oxide; it belongs to the class of NO-releasing drugs as a result. This drug is used as a vasodilator to reduce blood pressure. Sodium nitroprusside is also used as an analytical reagent for the detection of methyl ketones, and for the detection of amines that are often found in illicit drugs. It is on the WHO Model List of Essential Medicines, the most important medications needed in a basic health system.[3]

Medical use[edit]

Sodium nitroprusside is primarily used as a vasodilator. It was first used in human medicine in 1928.[4] By 1955, data on its safety during short-term use in patients with severe hypertension had become available.[4] Despite this, due to difficulties in its chemical preparation, it was not finally approved by the US FDA until 1974 for the treatment of severe hypertension.[4] By 1993, its popularity had grown such that total sales in the US had totalled US$2 million.[4]

Sodium nitroprusside has potent vasodilating effects in arterioles and venules (arterioles more than venules, but this selectivity is much less marked than that of nitroglycerin, which acts preferentially at venous smooth muscle) as a result of its breakdown to nitric oxide (NO).[5][6][7] It is intravenously infused in cases of acute hypertensive crises.[5][8] Its therapeutic effects are usually seen within a few minutes.[1]

Nitric oxide reduces both total peripheral resistance and venous return, thus decreasing both preload and afterload. So, it can be used in severe congestive heart failure where this combination of effects can act to increase cardiac output. In situations where cardiac output is normal, the effect is to reduce blood pressure.[5][6] It is sometimes also used to induce hypotension (to reduce bleeding) for surgical procedures (for which it is also FDA, TGA, and MHRA labelled).[5][8][9]

This compound has also been successfully used as a treatment for aortic valve stenosis,[10] erythromelalgia,[11] oesophageal varices,[12] severe pyrexia (fever),[13] lactic acidosis,[14] myocardial infarction,[15] neuroleptic malignant syndrome,[16] pulmonary hypertension,[17][18][19] respiratory distress syndrome in the newborn,[20][21] shock,[21] cerebral vasospasm,[22][23] ergot toxicity,[24][25][26][27] and ventricular septal defects.[28]

Adverse effects[edit]

Adverse effects by incidence and severity[5][6][7]


Unknown frequency

  • Nausea
  • Retching
  • Anxiety
  • Chest discomfort
  • Paraesthesial warmth
  • Abdominal pain
  • Orthostatic hypotension
  • ECG changes
  • Skin irritation
  • Flushing
  • Injection site erythema
  • Injection site streaking



Sodium nitroprusside should not be used for compensatory hypertension (e.g. due to an anteriovenous stent or coarctation of the aorta).[6] It should not be used in patients with inadequate cerebral circulation or in patients who are near death. It should not be used in patients with vitamin B12 deficiency, anaemia, severe renal disease, or hypovolaemia.[6] Patients with conditions associated with a higher cyanide/thiocyanate ratio (e.g. congenital (Leber's) optic atrophy, tobacco amblyopia) should only be treated with sodium nitroprusside with great caution.[6] Its use in patients with acute congestive heart failure associated with reduced peripheral resistance is also not recommended.[6] Its use in hepatically impaired individuals is also not recommended, as is its use in cases of pre-existing hypothyroidism.[5]

Its use in pregnant women is advised against, although the available evidence suggests it may be safe, provided maternal pH and cyanide levels are closely monitored.[6][29] Some evidence suggests sodium nitroprusside use in critically ill children may be safe, even without monitoring of cyanide level.[30]


The only known drug interactions are pharmacodynamic in nature, that is it is possible for other antihypertensive drugs to reduce the threshold for dangerous hypotensive effects to be seen.[6]


Due to its cyanogenic nature, overdose may be particularly dangerous. Treatment of sodium nitroprusside overdose includes the following:[6][31]

  • Discontinuing sodium nitroprusside administration
  • Buffering the cyanide by using sodium nitrite to convert haemoglobin to methaemoglobin as much as the patient can safely tolerate
  • Infusing sodium thiosulfate to convert the cyanide to thiocyanate.

Haemodialysis is ineffective for removing cyanide from the body but it can be used to remove most of the thiocyanate produced from the above procedure.[6]


The cyanide can be detoxified by reaction with a sulfur-donor such as thiosulfate, catalysed by the enzyme rhodanese.[32] In the absence of sufficient thiosulfate, cyanide ions can quickly reach toxic levels.[32]

Species LD50 (mg/kg) for oral administration[33] LD50 (mg/kg) for IV administration[6] LD50 (mg/kg) for skin administration[33]
Mouse 43 8.4  ?
Rat 300 11.2 >2000
Rabbit  ? 2.8  ?
Dog  ? 5  ?

Mechanism of action[edit]

Sodium nitroprusside breaks down in circulation to release nitric oxide (NO).[4] It does this by binding to oxyhaemoglobin to release cyanide, methaemoglobin and nitric oxide.[4] NO activates guanylate cyclase in vascular smooth muscle and increases intracellular production of cGMP. cGMP activates protein kinase G which activates phosphatases which inactivate myosin light chains.[34] Myosin light chains are involved in muscle contraction. The end result is vascular smooth muscle relaxation, which allow vessels to dilate.[34] This mechanism is similar to that of phosphodiesterase 5 (PDE5) inhibitors such as sildenafil (Viagra) and tadalafil (Cialis), which elevate cGMP concentration by inhibiting its degradation by PDE5.[35]

A role for NO in various common psychiatric disorders including schizophrenia,[36][37][38][39] bipolar disorder[40][41][42] and major depressive disorder[43][44][45] has been proposed and supported by several clinical findings. These findings may also implicate the potential of drugs that alter NO signalling such as SNP in their treatment.[38][44] Such a role is also supported by the findings of the recent SNP clinical trial.[46]

Structure and properties[edit]

Structure of sodium nitroprusside in the solid state, obtained by neutron diffraction

Nitroprusside is a complex anion that features an octahedral iron(III) centre surrounded by five tightly bound cyanide ligands and one linear nitric oxide ligand (Fe-N-O angle = 176.2 °[47]). The anion possesses idealized C4vsymmetry.

Nitric oxide is a non-innocent ligand. Due to the linear Fe-N-O angle, the relatively short N-O distance of 113 pm[47] and the relatively high stretching frequency of 1947 cm−1, the complex is formulated as containing an NO+ ligand.[48] Consequently, iron is assigned an oxidation state of 2+. The iron center has a diamagnetic low-spin d6 electron configuration, although a paramagnetic long-lived metastable state has been observed by EPR spectroscopy.[49]

The chemical reactions of sodium nitroprusside are mainly associated with the NO ligand.[50] For example, addition of S2− ion to [Fe(CN)5(NO)]2− produces the red [Fe(CN)5(NOS)]4− ion, which is the basis for a sensitive test for S2− ions. An analogous reaction also exists with OH ions, giving [Fe(CN)5(NO2)]4−.[48] Roussin's red salt (K2[Fe2S2(NO)4]) and Roussin's black salt (NaFe4S3(NO)7) are related iron nitrosyl complexes. The former was first prepared by treating nitroprusside with sulfur.[51]

This compound decomposes to sodium ferrous ferrocyanide, sodium ferrocyanide, nitric oxide, and cyanogen at about 450 °C. It decomposes in aqueous acid to liberate hydrocyanic acid (HCN).[52] Shielded from light, the concentrated solution is stable for more than two years at room temperature. It breaks down rapidly upon exposure to light, although the details are poorly understood. It degrades when heated (e.g. by sterilization in an autoclave), but addition of citric acid is helpful.[53]


Sodium nitroprusside can be synthesized by digesting a solution of potassium ferrocyanide in water with nitric acid, followed by neutralization with sodium carbonate:[54]

K4[Fe(CN)6] + 6 HNO3 → H2[Fe(CN)5(NO)] + CO2 + NH4NO3 + 4 KNO3
H2[Fe(CN)5NO] + Na2CO3 → Na2[Fe(CN)5(NO)] + CO2 + H2O

Alternatively, ferrocyanide may be oxidized with nitrite as well:[48]

[Fe(CN)6]4− + H2O + NO2 → [Fe(CN)5(NO)]2− + CN + 2 OH

Analytical reagent[edit]

Sodium nitroprusside was found by Legal to give a reaction with acetone or creatine under basic conditions in 1882. Rothera refined this method by the use of ammonia in place of sodium or potassium hydroxide. The reaction was now specific for methyl ketones. Addition of ammonium salts (e.g. ammonium sulfate) improved the sensitivity of the test, too.[55]

In this test, known as Rothera's test, methyl ketones (CH3C(=O)-) under alkaline conditions give bright red coloration (see also iodoform test). Rothera's test was initially applied to detecting ketonuria (a symptom of diabetes) in urine samples. This reaction is now exploited in the form of urine test strips (e.g. "Ketostix").[56]

Sodium nitroprusside is used in a separate urinalysis test known as the cyanide nitroprusside test or Brand's test. In this test, sodium cyanide is added first to urine and let stand for about 10 minutes. In this time, disulfide bonds will be broken by the released cyanide. The destruction of disulfide bonds liberates cysteine from cystine as well as homocysteine from homocystine. Next, sodium nitroprusside is added to the solution and it reacts with the newly freed sulfhydryl groups. The test will turn a red/purple colour if the test is positive, indicating significant amounts of amino acids were in the urine (aminoaciduria). Cysteine, cystine, homocysteine, and homocystine all react when present in the urine when this test is performed. This test can indicate inborn errors of amino acid transporters such as cystinuria, which results from pathology in the transport of dibasic amino acids.[57]

Sodium nitroprusside is also able to detect amines. This compound is thus used as a stain to indicate amines in thin layer chromatography.[58] Sodium nitroprusside is similarly used as a presumptive test for the presence of alkaloids (amine-containing natural products) common in illicit substances.[59] The test, called Simon's test, is performed by adding 1 volume of a solution of sodium nitroprusside and acetaldehyde in deionized water to a suspected drug, followed by the addition of 2 volumes of an aqueous sodium carbonate solution. The test turns blue for some secondary amines. The most common secondary amines encountered in forensic chemistry include 3,4-methylenedioxymethamphetamine (MDMA, the main component in Ecstasy) and phenethylamines such as methamphetamine. Sodium nitroprusside is also useful in the identification the mercaptans (thiol groups) in the nitroprusside reaction.

Other uses[edit]

Sodium nitroprusside spectrum is used to calibrate Mössbauer spectrometers

Sodium nitroprusside is often used as a reference compound for the calibration of Mössbauer spectrometers.[52] Sodium nitroprusside crystals are also of interest for optical storage. For this application, sodium nitroprusside can be reversibly promoted to a metastable excited state by blue-green light, and de-excited by heat or red light.[60]

In physiology research, sodium nitroprusside is frequently used to test endothelium-independent vasodilation. Iontophoresis, for example, allows local administration of the drug, preventing the systemic effects listed above but still inducing local microvascular vasodilation. Sodium nitroprusside is also used in microbiology, where it has been linked with the dispersal of Pseudomonas aeruginosa biofilms by acting as a nitric oxide donor.[61][62]


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