Atropine treatment before electroconvulsive therapy (ECT) is used for two main reasons: a) to prevent transient post-ictal bradyarrhythmias due to excessive vagal tone; b) to minimize secretions within the respiratory tract. In the present study we have compared the effects of premedication using atropine, a non-selective muscarinic antagonist, with biperiden, an M1-selective muscarinic antagonist. Cardiac rate and other cardiac parameters and respiratory tract secretions after ECT were compared in order to determine whether atropine effects following ECT involve central or peripheral antagonistic effects. Our results show that in preventing excessive sialorrhea following ECT, atropine works antagonistically through peripheral glandular M2 receptors whereas biperiden antagonizing M1 receptors fails to prevent sialorrhea. Our results are not conclusive concerning cardiac protective effects of atropine following ECT. None of the patients, whether premedicated by atropine or biperiden, displayed bradyarrhythmias following ECT. No significant differences were found in any of the measured cardiac parameters following ECT between atropine and biperiden premedications. Thus, the question whether atropine exerts its protective cardiac effects following ECT through central (probably M1) or peripheral M2 receptors remains open.