OBJECTIVE Atrial arrhythmias are prevalent during clinically abnormal myocardial loading, e.g. when the atrium is dilated or stretched. The initiating cause of the first premature beat that leads to this arrhythmia is unclear, as are the reasons for sustaining it. One possibility is that abnormal mechanical factors induce electrophysiological changes conductive to arrhythmia via 'mechanoelectric feedback'. The aim of this study is to investigate the concept that atrial stretch modulates the electrophysiological properties of the atrium via mechanoelectric feedback, and that mechanoelectric feedback can produce atrial arrhythmias. METHODS Guinea-pigs were humanely killed by cervical dislocation and the hearts removed and perfused with oxygenated Krebs-Henseleit solution by the Langendorff method. The heart was paced at an atrial site near the sinus node. Monophasic action potentials and electrocardiograms were recorded form the left atrium and left ventricle with suction electrodes. Transient stretch was induced by inflating a fluid-filled intra-atrial latex balloon catheter. RESULTS Increase in atrial volume produced several significant changes in the epicardial monophasic action potentials. It produced (i) decreases in the amplitude; (ii) a decrease in duration from 62.55 to 51.95 ms measured at 50% repolarisation (10.6 +/- 3.6 ms, P < 0.05, n = 6); (iii) an increase in duration from 122.45 to 140 ms measured at 90% repolarisation (17.55 +/- 4.5 ms, P < 0.05, n = 6) --due to the presence of early afterdepolarisations. (iv) These load-induced electrophysiological changes coincided with the occurrence of arrhythmia or premature atrial beats. CONCLUSIONS Load changes in the atrium can produce electrophysiological changes of a kind that may be relevant to clinical atrial arrhythmia.