Both impulsivity and stress are risk factors for substance abuse, but it is not clear how these two processes interact to alter susceptibility for the disorder. The aim of this project was to examine the pharmacology of a stress–impulsivity interaction in rats. To do so, we tested the effects of yohimbine on impulsive action and then assessed whether behavioural changes could be reduced by antagonists at different receptor subtypes. Male Long–Evans rats were injected with various doses of yohimbine (0–5.0 mg/kg) before testing in the response-inhibition task. In subsequent experiments, yohimbine (2.5 mg/kg) was injected following pretreatment with the following receptor antagonists: corticotropin-releasing factor receptor 1, antalarmin (0–20 mg/kg); glucocorticoid, mifepristone (0–30 mg/kg); noradrenergic (NA) α1, prazosin (0–2 mg/kg); NA α2, guanfacine (0–0.5 mg/kg); NA β2, propranolol (0.5–2.0 mg/kg); dopamine D1/5, SCH 39166 (0–0.0625 mg/kg); μ opioid, naloxone (0–2 mg/kg); or 5-HT2A, M100907 (0.005–0.05 mg/kg). In all experiments, impulsive action was measured as increased premature responding. Yohimbine dose dependently increased impulsive action, but the effect was not reversed by antagonist pretreatment. None of the drugs altered any other behavioural measure. We conclude that stress–impulsivity interactions are likely mediated by a synergy of multiple neurotransmitter systems.