Background: Diabetics have increased risk of cardiovascular complications including arrhythmia. The underlying mechanisms likely include fibrosis, changes in cell size, remodeling of ion channels, and gap junctions but data are contradictory and possibly model dependent. The aim of the present study was to investigate conduction velocity (CV) and its sensitivity to ischemia in strips of right ventricles of Zucker Diabetic Fatty (ZDF) rats, a model of type 2 diabetes. Furthermore, we tested the ability of the anti-arrhythmic peptide analogue AAP10 to improve CV. Results: CV was significantly slower in ZDF rats (56 cm/s) compared to non-diabetic controls (ZDL, 66 cm/s) and CV in ZDF rats were more sensitive to ischemia induced by reduced chamber flow (ZDF 39 % and ZDL 28 % reduction). The total amount of connexin 43 (Cx43) was unchanged; however, the amount of lateralized Cx43 was significantly increased in ZDF rats. The phosphorylation state of Cx43, judged by electrophoretic mobility, was unchanged in ZDF compared to ZDL rats although this does not rule out that the phosphorylation of some sites may differ. Measurement of phosphorylation after ischemia and reperfusion showed that the fraction migrating as the P0 band increased significantly in both groups. No hypertrophy, judged by differences in cell length or cell area, was observed in ZDF compared to ZDL rats. Stimulation with AAP10 had no effect on CV during baseline conditions in either ZDF or ZDL rats. During ischemia CV was reduced significantly in both ZDF and ZDL rats and the CV slowing was partially prevented by AAP10. Conclusion: CV and the conduction reserve are reduced in ZDF rats. Lateralization of Cx43 is increased in ZDF rats and since lateralized Cx43 is probably not functional, this may partly explain the reduced CV. Independent of disease AAP10 partially prevented CV slowing during ischemia suggesting that gap junctions are partly involved in this response.