Angiogenesis is an important adaptive mechanism to maintain capillary density during cardiac hypertrophic growth and ensure oxygen and nutrition supply. Aldosterone and the mineralocorticoid receptor (MR) are key drivers of adverse cardiovascular remodeling. Using a cell type-specific deletion model we show here that endothelial cell MR activation impaired angiogenesis. RNAseq from endothelial cells revealed opposing effects of aldosterone and VEGF on gene expression. This was associated with an upregulation of the vascular endothelial cell growth factor (VEGF) receptor 2 in MR-deficient endothelial cells.