Nitroprusside breaks down in circulation to become nitric oxide (NO). Downstream effects of NO in the blood are venodilation and vasodilation.
As a result of increased NO, guanyl cyclase is activated in smooth muscle, increasing cGMP production. This increase in cGMP inactivates myosin light chains and causes smooth muscle relaxation, or arteriodilation. This drug is a potent dilator of venules and arterioles.
This drug has a half-life of 1-2 minutes and is rapidly acting.
Nitroprusside is administered intravenously to treat malignant hypertension. Malignant hypertension, or hypertensive emergency, is a serious condition characterized by an extremely high blood pressure which acutely impairs one or more organ systems.
Nitroprusside administration can lead to iatrogenic cyanide toxicity if overused. Sodium nitroprusside has 5 CN ligands in its molecule, and breaks down into thiocyanate. This is usually detoxified in the blood, but can reach toxic levels in the blood. Common toxicity symptoms include vertigo, confusion, difficulty breathing and headaches at low doses.
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