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Antagonists at the L-type voltage sensitive calcium channel (L-VSCC) potentiate anesthetic potency in experimental models, suggesting that it may be a target site for IV anesthetics. Nimodipine is a 1,4-dihydro- pyridine antagonist of L-VSCC which crosses the blood-brain barrier. We tested the hypothesis that premedication with oral nimodipine in healthy patients would reduce the induction dose of propofol, independently of its effects on the cerebral circulation. Sixty ASA physical status I or II patients (18–60 yr), undergoing knee arthroscopy or minor urological surgery, were randomized to receive either nimodipine 60 mg or placebo, orally 1–2 h before induction. Noninvasive mean blood pressure, heart rate, and time-averaged mean velocity in the middle cerebral artery by using transcranial Doppler ultrasonography were obtained before and 5 min after the induction of anesthesia. Propofol 1% was administered by an infusion pump at a rate of 10 mL/min. Both groups of patients had a reduction in mean blood pressure after the induction (P < 0.01), but there were no significant differences between the groups. The induction dose of propofol was 2.19 mg/kg (95% confidence interval [CI]: 1.97–2.42) in the nimodipine group, compared with 2.16 mg/kg (95% CI 1.98–2.34) in the control group, P = 0.8. Time-averaged mean velocity remained unchanged after the induction of anesthesia in both patients receiving nimodipine premedication (51% CI 43–59 cm/s to 52% CI 46–58 cm/s, P = 0.6) and those receiving placebo (50% CI 43–58 cm/s to 53% CI 45–59 cm/s, P = 0.3). Premedication with oral nimodipine 60 mg does not reduce the induction dose of propofol compared with placebo, casting doubt on the hypothesis that propofol has an anesthetic action at L-VSCC.Premedication with oral nimodipine 60 mg does not reduce the induction dose of propofol compared with placebo, casting doubt on the hypothesis that propofol has an anesthetic action at L-type voltage sensitive calcium channels.