Chronic volume overload to the heart has been suggested to generate arrhythmic substrates in the atria, leading to the onset of atrial fibrillation (AF). We investigated a role of TRPC channels in the pathophysiological process of atrial remodelings caused by aorto-venocaval shunt (AVS) in rats. More than 3 months after the surgery, the atrial weight of the AVS group (n = 10) was greater than that in the Sham group (n = 9), and fibrosis was observed in the atrial tissue. The P-wave duration, PR interval and QRS width of the ECG were significantly prolonged in the AVS group compared with those in the Sham group. The duration of AF induced by burst pacing in the AVS group was about 4 times longer than that in the Sham group. The mRNA levels of TRPC channel in the AVS group were significantly greater than those in the Sham group. Chronic administration of a TRPC 3 channel inhibitor pyrazole-3 to the AVS rats ameliorated the prolongation of the P-wave duration and QRS width caused by AVS surgery. Furthermore, the duration of AF was significantly shortened by the drug to the same level as the Sham group. These results suggest that TRPC3 channel is involved in the atrial remodeling caused by chronic volume overload.