Potentiated effects of alcohol, sedatives, hypnotics or other centrally-active substances. Reduced therapeutic effect by NSAIDs. Abolished α
2-adrenergic receptor-mediated effects w/ α
2-adrenergic receptor blockers eg, phentolamine. Potentiated bradycardic rhythm disturbances w/ β-blockers, digitalis glycosides. Potentiated peripheral vascular disorders by β-blockers. Reduced or abolished effects & provoked or aggravated orthostatic regulation disturbances w/ TCAs, neuroleptics w/ α-receptor blockers. Increased arrhythmogenic potential of high-dose IV haloperidol.