The A(2A)R (adenosine 2A receptor) plays a crucial role in the pathophysiological process of cardiovascular diseases, yet its effect on aortic remodeling remains unclear. We observed elevated adenosine and A(2A)R levels following infusion of mice with Ang II (angiotensin II), suggesting a potential role for the adenosine-A(2A)R system in macrophage accumulation and subsequent aortic remodeling. The effects and mechanisms of A(2A)R on macrophage dynamics during aortic remodeling were further investigated using mice with macrophage knockout of A(2A)R and by transplantation of A(2A)R(-/-) bone marrow. We demonstrated that macrophage knockout of A(2A)R inhibited macrophage accumulation and subsequent aortic remodeling by inhibiting macrophage retention. This was shown to occur via promotion of macrophage emigration to the draining lymph node. These effects correlated with restoration of the expression and surface content of CCR7 (CC chemokine receptor 7). Consistently, A(2A)R(-/-) bone marrow transplantation relieved Ang II-induced aortic remodeling, macrophage retention, and CCR7 downregulation and internalization, all of which were rescued by A(2A)R(+)/(+) bone marrow transplantation. In addition, CCR7 antibody treatment blocked all the protective effects observed in A(2A)R-cKO mice, including attenuation of aortic remodeling and decreased macrophage retention. In in vitro studies, A(2A)R activation induced by Ang II suppressed macrophage migration to CCL19 (CC-chemokine ligand) 19 through downregulation and internalization of CCR7. In summary, A(2A)R activation contributes to Ang II-induced macrophage retention and subsequent aortic remodeling by inhibiting migration of macrophages to the draining lymph node through regulating CCR7 expression and internalization.