Microvascular endothelial cells are protagonists in inflammation and angiogenesis. Since magnesium (Mg) deficiency promotes inflammation and impairs angiogenesis in vivo, we evaluated the effect of different concentrations of the cation on microvascular 1G11 cells. We found that low Mg inhibits endothelial growth and migration, while it increases some inflammatory markers. In particular we show that low Mg stimulates the synthesis of interleukin 1a and 6, of nitric oxide, a mediator of inflammatory responses, and of VCAM, which mediates monocyte/endothelial interactions. On the contrary, high Mg stimulates proliferation and migration and sensitizes microvascular cells to migratory signals, thus inducing crucial events in angiogenesis. Our results demonstrate a direct role of Mg in modulating microvascular functions and provide a molecular explanation to the link among Mg, angiogenesis and inflammation observed in in vivo models.