1. Effects of the parasympathetic neuromediator acetylcholine (ACh) on atrial tissues vary greatly depending on the species, the type of atrial cells and experimental conditions. The aim of the present study was to investigate, with microelectrode techniques, the arrhythmogenic effects of ACh in tilapia (Oreochromis sp.) isolated atria at room (22-25 degrees C) and high temperature (37 degrees C). 2. Acetylcholine (1-10 micromol/L) shortened action potential duration (APD), depressed action potential plateau and decreased twitch force in tilapia atria, as it did in human atrial fibres. In addition, ACh induced premature responses and re-entrant tachyarrhythmias (TA; frequency range from 7 to 25 Hz) in five of 19 and 14 of 22 tilapia atria tested at room and high temperature, respectively. The higher incidence of ACh-induced TA at 37 degrees C compared with room temperature was statistically significant. 3. The ACh-induced TA consisted of high-frequency and uniform action potentials accompanied by tension oscillation and elevation of diastolic force (flutter). Acetylcholine-induced TA could be readily abolished by atropine (1 micromol/L) and prevented by treatment with agents with local anaesthetic properties, such as 0.1 micromol/L tetrodotoxin or 3 micromol/L quinidine. The antagonistic action of quinidine occurred without significant prolongation of APD. 4. The present findings suggest that pharmacological concentrations of the cholinergic muscarinic agonist ACh readily induce TA (mainly atrial flutter) in tilapia atria, presumably via sodium channel-dependent re-entrant excitation. The poikilothermic tilapia appears to be an appropriate animal model for the study of atrial TA.