Nimodipine; Mechanism, Uses, Contraindications, Dosage, Side effects,

Nimodipine; Mechanism, Uses, Contraindications, Dosage, Side effects,

Nimodipine is a dihydropyridine derivative and an analog of the calcium channel blocker nifedipine, with antihypertensive activity. Nimodipine inhibits the transmembrane influx of calcium ions in response to depolarization in smooth muscle cells, thereby inhibiting vascular smooth muscle contraction and inducing vasodilatation. Nimodipine has a greater effect on cerebral arteries than on peripheral smooth muscle cells and myocardial cells, probably because this agent can cross the blood-brain barrier due to its lipophilic nature. Furthermore, this agent also inhibits the drug efflux pump P-glycoprotein, which is overexpressed in some multi-drug resistant tumors, and may improve the efficacy of some antineoplastic agents.

Nimodipine is a dihydropyridine calcium channel blocker originally developed for the treatment of high blood pressure. It is not frequently used for this indication, but has shown good results in preventing a major complication of subarachnoid hemorrhage (a form of cerebral hemorrhage) termed vasospasm; this is now the main use of nimodipine. Nimodipine is a 1,4-dihydropyridine calcium channel blocker. It acts primarily on vascular smooth muscle cells by stabilizing voltage-gated L-type calcium channels in their inactive conformation. By inhibiting the influx of calcium in smooth muscle cells, nimodipine prevents calcium-dependent smooth muscle contraction and subsequent vasoconstriction. Compared to other calcium channel blocking agents, nimodipine exhibits greater effects on cerebral circulation than on peripheral circulation.

 Mechanism of action of Nimodipine

Nimodipine binds specifically to L-type voltage-gated calcium channels. There are numerous theories about its mechanism in preventing vasospasm, but none are conclusive. Nimodipine has additionally been found to act as an antagonist of the mineralocorticoid receptor, or as an antimineralocorticoid. Although the precise mechanism of action is not known, nimodipine blocks the intracellular influx of calcium through voltage-dependent and receptor-operated slow calcium channels across the membranes of myocardial, vascular smooth muscle, and neuronal cells. Nimodipine binds specifically to L-type voltage-gated calcium channels. The inhibition of calcium ion transfer results in the inhibition of vascular smooth muscle contraction. Evidence suggests that the dilation of small cerebral resistance vessels, with a resultant increase in collateral circulation, and/or a direct effect involving the prevention of calcium overload in neurons may be responsible for nimodipine’s clinical effect in patients with subarachnoid hemorrhage.

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Indications of Nimodipine

  • Hunt and Hess Grades I-V Subarachnoid hemorrhage
  • Subarachnoid Hemorrhage
  • Ischemic Stroke
  • Migraine Prevention
  • Treatment of aneurysmal subarachnoid hemorrhage
  • For use as an adjunct to improve neurologic outcome following subarachnoid hemorrhage (SAH) from ruptured intracranial berry aneurysms by reducing the incidence and severity of ischemic deficits.

Dosage of Nimodipine

Strengths: 30 mg; 60 mg/20 mL; 30 mg/10 mL

 Subarachnoid Hemorrhage

  • 60 mg orally, nasogastric, or gastric tube every 4 hours
  • Duration of therapy: 21 days

Side Effects of Nimodipine

The most common 

More common


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Drug Interactions of Nimodipine

Nimodipine  may interact with following drugs, supplements, & may change the efficacy of drug

Pregnancy Category

FDA Pregnancy Category C


This medication should not be taken by women who are or may become pregnant, as nimodipine may cause harm to the developing baby if it is taken by the mother during pregnancy. If you become pregnant while taking this medication, contact your doctor immediately.


This medication should not be taken by women who are breast-feeding. The safety and effectiveness of using this medication have not been established for children.

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