Although acute atrial dilation facilitates the induction of atrial fibrillation (AF) in the normal heart, little is known about whether the induction of AF due to acute atrial dilation increases in the diseased heart. To clarify this, we compared the inducibility of AF by an acute increase of atrial pressure with and without chronic atrial dilation induced by volume- and pressure-overload in rats. Eight weeks after creating abdominal aortocaval shunt and aortic constriction rats (LVH rats, n = 8) or sham rats (n = 8), the hearts were perfused in Langendorff's manner. Right atrial (RA) pressure was increased from 2 cm H(2)O to 10 cm H(2)O by the height of the reservoir. Inducibility of AF was evaluated by 5 times burst pacing from the right atrium, and mean cycle length of AF (CL) and the atrial effective refractory period (AERP) were also measured. The inducibility of AF increased from 5 ± 3% at 2 cm H(2)O to 50 ± 5% at 10 cm H(2)O RA pressure in sham rats (P < 0.01), but not in LVH rats (20 ± 7% to 25 ± 6%, NS). Mean CL and AERP in LVH rats were longer than those in sham rats. In addition, the AERP decreased with an increase in RA pressure from 2 cm H(2)O to 10 cm H(2)O in sham rats, but not in LVH rats. The inducibility of AF caused by an acute increase of RA pressure did not increase in the diseased heart, suggesting that electrophysiological remodeling may play a role, at least in a compensated state, for the prevention of AF due to an acute increase of atrial pressure.