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Acute and chronic kidney disease are two of the most commonly diagnosed kidney dysfuctions in both human and companion animals. The characteristics of an injured kidney include an increase of blood urea nitrogen, serum creatinine and a decrease of glomerular filtration rate. At the cellular level, infiltration of inflammatory cells, disruption of kidney epithelial cell lining and increased amount of type IV collagen have all been reported. Retrospective studies from human patients revealed a positve correlation between higher level of serum vasopressin and disease progression; however, the actual mechanism underlying vasopressin effect on kidney disease progression remains to be elucidated. In this study, we demonstrated that arginine vasopressin not only stimulates the de-polymerization of F-actin, but also promotes redistribution of adhesion junction protein E-Cadherin which is likely to be respoinsible for the lost of regular epithelial cell polarity in kidney tubules. Our data supported the detrimental effects of vasopressin on kidney epithelial cells and provided evidences on the potential cause and consequence relationship between patients with higer serum vasopressin concentration with the accelerated kidney tubule disruption.