Substantial evidence implicates dopaminergic neural systems in the occurrence of polydipsia in both animals and humans. Two experiments were conducted in order to specify the behavioral mechanisms whereby manipulation of dopaminergic neural transmission can affect scheduled-induced polydipsia (SIP). The role of dopamine D1 and D2 receptors was investigated by comparing the behavioral effects of dopamine D1 agonists (SKF 38393 and SKF 82958) and antagonists (SCH 23390 and SKF 83566) to those of a dopamine D2 agonist (quinpirole) and antagonist (haloperidol) by using an animal model of excessive water consumption, drinking evoked in the SIP paradigm. Additionally, the behavioral effects of these relatively specific compounds were compared to those of the indirect agonist d-amphetamine sulfate and the nondopaminergic drug, diazepam. All of the drugs produced dose-related decreases in SIP. With the exception of SKF 38393 and SCH 23390, the decreased drinking appeared to be a behaviorally nonspecific drug effect in that changes in activity consistently preceded or accompanied reductions in water consumption. Some of the drugs tested, including quinpirole, haloperidol and SKF 83566, also produced changes in behavior consistent with decreased hunger, which may have also contributed to the reductions in SIP. These results are generally suggestive that dopamine neural systems are involved mainly in the motor or performance aspects of established SIP and that disruptions in established SIP produced by dopamine agonists or antagonists may result from a change in the balance of activation of dopamine D1 and D2 receptors. These results may be relevant to understanding the factors influencing polydipsia in humans.