Background Mechanical stretch has been shown to induce vascular remodeling and increase vessel density, but the pathophysiological mechanisms as well as the morphological changes induced by tensile forces to dermal vessels are poorly understood. Methods A custom computer controlled stretch device was designed and applied to the backs of C57BL/6 mice (n=38). Dermal and vascular remodeling was studied over a 7 days period. Corrosion casting and three-dimensional (3D) scanning electron microscopy (SEM) as well as CD-31 staining were performed to analyze microvessel morphology. Hypoxia was assessed by immunhistochemistry. Western blot analysis of VEGF and mRNA expression of VEGF receptors were performed. Results Skin stretching was associated with increased angiogenesis as demonstrated by CD31 staining and vessel corrosion casting where intervascular distance and vessel diameter were decreased (p<0.01). Immediately after stretching VEGF dimers were increased. mRNA expression of VEGFR1, VEGFR2, NP1 and NP2 were increased starting as early as 2 hours after stretching. Highly proliferating epidermal cells induced epidermal hypoxia starting at day 3 (p<0.01). Conclusion Identification of significant hypoxic cells occurred after identification of neovessels suggesting an alternative mechanism. Increased expression of angiogenic receptors, stabilization of VEGF dimers may be involved in a mechanotransductive, prehypoxic induction of neovascularization.