The long-term pathomorphological changes of the injured vessels under angiotensin-converting-enzyme (ACE) inhibitor are still not known. Therefore, we assessed the alternations of vascular architecture after three-month therapy with ACE inhibitor and identified new target cells for this medication. Carotid arteries of spontaneously hypertensive rats underwent balloon angioplasty. 14 days prior intervention, half of the animals was treated with ACE inhibitor. After three months of vascular trauma, the injured vessels were explored by histomorphology and immunohistochemistry for angiotensin-II receptor (AT1R), dendritic and HSP47+ cells. The neointimal growth decreased significantly only up to 28 days under ACE inhibitor. In contrast, the reductive effect of ACE inhibitor on media area persisted up to three months after intervention. A significant fraction of early neointimal cells was of a dendritic cell type. The relevant portion of these cells showed an expression of AT1R and HSP47. AT1R was present in 70% and HSP47 in 18% of all early neointimal cells in both groups. ACE inhibitor may at least temporarily diminish remodelling processes in injured vessels. The detection of AT1R on dendritic cells identifies these cells as important targets for therapeutic strategies involving modulation of the renin-angiotensin system.