Nimodipine, a dihydropyridine calcium channel blocker, relaxes smooth muscle by inhibiting the influx of calcium ions through voltage-operated channels in the cell membrane. It seems to act preferentially on cerebral vessels rather than peripheral vessels. The actual mechanism of action in humans is uncertain. While some studies have demonstrated increases in cerebral blood flow, a recent small angiographic study in patients with subarachnoid haemorrhage found no significant difference in cerebral blood flow. Angiographically demonstrated moderate to severe vasospasm was not significantly altered by nimodipine; however, neurological status has been shown to improve even in patients without vasospasm.

Although oral nimodipine is rapidly and almost completely absorbed, bioavailability is low and variable because of extensive first-pass metabolism.

Adverse effects of oral nimodipine include dose-dependent hypotension, flushing, feeling of warmth, headache, diarrhoea, rash, oedema, bradycardia, nausea and vomiting. Adverse effects of intravenous nimodipine include hypotension, headache and extrasystoles. Intravenous nimodipine is administered via a central vein because of the risk of phlebitis.