Enhancement of a vecuronium neuromuscular blockade by prior administration of succinylcholine has been attributed to both pharmacokinetic and pharmacodynamic mechanisms. This study was performed to elucidate the mechanism of this interaction using decamethonium as the agonist drug. In five healthy patients undergoing gynecologic surgery, a cumulative dose-response relationship to vecuronium was determined following recovery from a neuromuscular block produced by 0.1 mg/kg intravenous decamethonium. In a second group of five similar patients, a cumulative dose-response curve to vecuronium was obtained without previous exposure to decamethonium. In this second group, at 30% recovery from a vecuronium block, 0.1 mg/kg decamethonium was administered. The results demonstrated a sevenfold increase in sensitivity (reducing the ED50 from 24 micrograms/kg to 3.5 micrograms/kg) to vecuronium when it was administered following recovery from decamethonium block, and a partial reversal lf the vecuronium block by decamethonium when the decamethonium was administered during recovery from vecuronium block. These findings support a pharmacodynamic explanation of the increased sensitivity to nondepolarizing muscle relaxants following recovery from an agonist neuromuscular block.