Endothelial permeability is regulated partly by cells adheren junctions (AJs), which opens and closes with the dynamic. In endothelial cells, AJs largely composed of vascular endothelial cadherin (VE-cadherin), cadherin family member that is a specific adhesion protein only in endothelial cells, through the cytoplasm domain binds to other proteins, including p120, catenin-β - and plakoglobin. In many ways the endogenous pathway increases vascular permeability by affecting the function and organization of VE-cadherin and other proteins at AJs. We will discuss some of the factors that can increase vascular permeability, including vascular endothelial growth factor (VEGF), induced tyrosine phosphorylation of VE-cadherin, which accompanies an increase in vascular permeability and leukocyte diapedesis, in addition, the internalization of VE-cadherin and splits can cause AJS being dismantled. Possible use of inhibitors of the SRC and other kinases, of agents that increase cAMP levels, and lytic enzyme inhibitors as pharmacological tools are to reduce endothelial permeability.