Alcohol and nicotine use disorders are often treated as separate diseases, despite evidence that approximately 80–90% of alcohol dependent individuals are also heavy smokers. Both nicotine and ethanol have been shown to interact with neuronal nicotinic acetylcholine receptors (nAChRs), suggesting these receptors are a common biological target for the effects of nicotine and ethanol in the brain. There are few studies that have examined the effects of co‐administered nicotine and ethanol on the activity of nAChRs in rodents. In the present study, we show that Sprague‐Dawley rats, a strain often used for nicotine studies but not as often for voluntary ethanol intake studies, will consume 20% ethanol using both the intermittent‐access two‐bottle‐choice and operant self‐administration models without the need for sucrose fading. We show that nicotine (0.2 mg/kg and 0.8 mg/kg, s.c.) significantly increases operant 20% ethanol self‐administration and varenicline (2 mg/kg, s.c), a partial agonist at nAChRs, significantly decreases operant ethanol self‐administration and nicotine‐induced increases in ethanol self‐administration. This suggests that nAChRs play an important role in increasing ethanol self‐administration and that varenicline may be an efficacious treatment for alcohol and nicotine co‐dependencies.