Exchange protein activated by cyclic AMP (Epac) -- a cyclic AMP-activated guanine nucleotide exchange factor for Ras-like GTPases -- has emerged as a novel mediator of pivotal processes in the cardiovascular system, including cellular calcium handling, hypertrophy, integrin-mediated cell adhesion, establishment of cell polarity, cell migration and endothelial barrier functioning. Epac controls these various cellular responses apparently by signaling to several effector proteins. Spatiotemporal dynamics in the subcellular distribution of Epac-driven signaling networks probably determine the net outcome of cyclic AMP signaling in the cardiovascular system.