14402-89-2 Usage
Description
Sodium nitroprusside, also known as sodium nitroferricyanide or disodium pentacyanonitrosylferrate(2), is a potent blood pressure-lowering drug that has been known for its antihypertensive effects since 1928. It is a reddish-brown, water-soluble powder that is decomposed by light when in solution. Sodium nitroprusside works by releasing nitric oxide (NO) spontaneously in the blood, causing vasodilation in both arterial and venous vascular beds. It is metabolized by the liver, yielding thiocyanate, which is excreted by the kidneys. Due to its short duration of action, its use is limited to hypertensive emergencies.
Uses
Used in Hypertensive Emergencies:
Sodium nitroprusside is used as a potent vasodilator for the treatment of hypertensive emergencies. It rapidly lowers blood pressure by causing peripheral vasodilation, which results from a direct effect on both arterial and venous vessels. This makes it an effective drug for managing severe hypertension in critical situations.
Used in Cardiology:
In the field of cardiology, sodium nitroprusside is used as a short-acting intravenous drug for managing acute heart failure and other conditions that require rapid blood pressure reduction. Its instantaneous action and ability to dilate both arterial and venous beds make it a valuable tool in the treatment of various cardiovascular conditions.
Used in Anesthesia:
Sodium nitroprusside is also used in anesthesia to control blood pressure during surgery. Its short-acting nature allows anesthesiologists to quickly and effectively manage blood pressure fluctuations that may occur during the procedure, ensuring the safety and stability of the patient.
Used in Research:
In addition to its clinical applications, sodium nitroprusside is used in research settings to study the effects of nitric oxide on vascular function and blood pressure regulation. Its ability to release nitric oxide spontaneously makes it a useful tool for investigating the role of this molecule in various physiological processes.
Biological Functions
Sodium nitroprusside (Nipride) is a potent directly acting
vasodilator capable of reducing blood pressure in all
patients, regardless of the cause of hypertension. It is
used only by the intravenous route for the treatment of
hypertensive emergencies. The pharmacological activity
is caused by the nitroso moiety. The actions of the drug
are similar to those of the nitrites and nitrates that are
used as antianginal agents. The action
of the nitrovasodilators depends on the intracellular
production of cGMP.
Mechanism of action
Sodium nitroprusside is not an active hypotensive drug until metabolized to its active metabolite, NO, the mechanism of
action of which has been previously described. Studies with sodium nitroprusside suggest that it releases
NO by its interaction with glutathione or with sulfhydryl groups in the erythrocytes and tissues to form a S-nitrosothiol
intermediate, which spontaneously produces NO, which in turn freely diffuses into the VSM, thereby increasing
intracellular cGMP concentration. NO also activates K+
channels, which leads to hyperpolarization and relaxation.
The hypotensive effect of sodium nitroprusside is augmented by concomitant use of other hypotensive agents and is
not blocked by adrenergic blocking agents. It has no direct effect on the myocardium, but it may exert a direct coronary
vasodilator effect on VSM. When sodium nitroprusside is administered to hypertensive patients, a slight increase in
heart rate commonly occurs, and cardiac output usually is decreased slightly. Moderate doses of sodium nitroprusside
in patients with hypertension produce renal vasodilation without an appreciable increase in renal blood flow or
decrease in glomerular filtration.
Intravenous infusion of sodium nitroprusside produces an almost immediate reduction in blood pressure. Blood
pressure begins to rise immediately when the infusion is slowed or stopped and returns to pretreatment levels within 1
to 10 minutes.
Pharmacology
In contrast to hydralazine, minoxidil, and diazoxide,
sodium nitroprusside relaxes venules as well as arterioles.
Thus, it decreases both peripheral vascular resistance
and venous return to the heart. This action limits
the increase in cardiac output that normally follows vasodilator
therapy. Sodium nitroprusside does not inhibit
sympathetic reflexes, so heart rate may increase following
its administration even though cardiac output is not increased. Renal blood flow remains largely unaffected
by sodium nitroprusside, because the decrease in renal
vascular resistance is proportional to the decrease in
mean arterial pressure. As with all vasodilators, plasma
renin activity increases.
Pharmacokinetics
Sodium nitroprusside undergoes a redox reaction that releases cyanide. The cyanide that is produced is rapidly
converted into thiocyanate in the liver by the enzyme thiosulfate sulfotransferase (rhodanase) and is excreted in the
urine. The rate-limiting step in the conversion of cyanide to thiocyanate is the availability of sulfur donors,
especially thiosulfate. Toxic symptoms of thiocyanate begin to appear at plasma thiocyanate concentrations of 50 to
100 mg/mL. The elimination half-life of thiocyanate is 2.7 to 7.0 days when renal function is normal but longer in
patients with impaired renal function.
Clinical Use
Sodium nitroprusside is used in the management of hypertensive
crisis. Although it is effective in every form
of hypertension because of its relatively favorable effect
on cardiac performance, sodium nitroprusside has special
importance in the treatment of severe hypertension
with acute myocardial infarction or left ventricular failure.
Because the drug reduces preload (by venodilation)
and afterload (by arteriolar dilation), it improves
ventricular performance and in fact is sometimes used
in patients with refractory heart failure, even in the absence
of hypertension.
Side effects
The most commonly encountered side effects of sodium
nitroprusside administration are nausea, vomiting, and
headache, which quickly dissipate when the infusion is
terminated. When sodium nitroprusside treatment extends
for several days, there is some danger of toxicity
owing to the accumulation of its thiocyanate metabolite.
Thiocyanate intoxication includes signs of delirium
and psychosis; hypothyroidism also may occur. If nitroprusside
is administered for several days, thiocyanate
levels should be monitored.
Close supervision is required when nitroprusside is
used because of the drug’s potency and short duration
of action.
Safety Profile
Human poison by inhalation and intravenous routes. Experimental poison by ingestion, intraperitoneal, and intravenous routes. Human systemic effects: increased intracranial pressure, general anesthesia, change in heart rate, and metabolic acidosis. An experimental teratogen. Used as a vasodilator for short-term treatment of severe hypertension. Mixtures with sodium nitrite explode when heated. When heated to decomposition it emits toxic fumes of NOx, CN-, and Na2O.
Synthesis
It is synthesized by successive reactions
including the reaction of potassium ferrocyanide with nitric acid, which forms potassium
nitroprusside (22.6.5), which is further transformed to copper nitroprusside (22.6.6), and
reaction of this with sodium carbonate gives sodium nitroprusside (22.6.7).
Drug interactions
Potentially hazardous interactions with other drugs
Anaesthetics: enhanced hypotensive effect.
Metabolism
The onset of the hypotensive action of sodium nitroprusside
is rapid, within 30 seconds after intravenous
administration. If a single dose is given, the action lasts
for only a couple of minutes. Therefore, sodium nitroprusside
must be administered by continuous intravenous
infusion. After the infusion is stopped, blood
pressure returns to predrug levels within 2 to 3 minutes.
Nitroprusside is metabolically degraded by the liver,
yielding thiocyanate. Because thiocyanate is excreted
by the kidney, toxicities due to this compound are most
likely in patients with impaired renal function.
Check Digit Verification of cas no
The CAS Registry Mumber 14402-89-2 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 1,4,4,0 and 2 respectively; the second part has 2 digits, 8 and 9 respectively.
Calculate Digit Verification of CAS Registry Number 14402-89:
(7*1)+(6*4)+(5*4)+(4*0)+(3*2)+(2*8)+(1*9)=82
82 % 10 = 2
So 14402-89-2 is a valid CAS Registry Number.
InChI:InChI=1/5CN.Fe.NO.2Na/c5*1-2;;1-2;;/q;;;;;2*-1;2*+1/rC5FeN6O.2Na/c7-1-6(2-8,3-9,4-10,5-11)12-13;;/q-2;2*+1
