Sodium Nitroprusside

It directly causes relaxation of the peripheral vessels.


Mechanism of action:
It causes the release of nitric oxide (NO). NO is a relaxing factor. NO stimulates guanylyl cyclase in vascular smooth muscle leading to vasodilatation.

When it acts on arterioles it causes a reduction in total systemic vascular resistance leading to a fall in blood pressure.

Actions:
It causes relaxation of smooth muscles of both arteries and veins resulting in the immediate vasodilatation with reflex tachycardia.

Cardiac rate is promoted in the supine position and reduced in the standing position. Cardiac rate is increased reflexly.

It results in reduced oxygen demand of the heart muscles caused by promoted venous capacitance.

It regulates the blood to the kidneys and there is a slightly promoted renin secretion.

Pharmacokinetics:
It is rapidly metabolized as its half life is about 2 minutes. Its metabolism causes the production of cyanide ions. It is eliminated by the kidney.

Therapeutic uses:
1. It is used in hypertensive crisis as it has the ability of reducing the blood pressure in standing as well as supine position.
2. It is used for reducing bleeding during surgery
3. It is used in ventricular unloading in acute congestive heart failure.
4. It is used for acute myocardial infarction

Adverse effects:
It may cause headache, excessive hypotension, tachycardia, agitation, palpitation, restlessness, nausea, cyanide ions poisoning (which can be treated by using sodium thiosulfate), disorientation, muscle spasms and convulsions.

Dosage and administration:
It is given by continuous IV infusion in the dose of 0.5-1.0 μg/kg/min.