To search for the barrier-improving agents that can protest against microvascular hyperpermeability during tumor growth and metastasis, the first aim of our study was to test the hypothesis that elevation of the intraendothelial cAMP levels also abolishes/attenuates the transient increase in microvascular permeability by a tumor angiogenic factor, VEGF, in intact microvessels. Here, VEGFA is linked to neoplasm.