Objective: Intimal thickening is an adaptive response to injury and to stimuli acting on the vessel wall. Vascular remodeling (VR) is defined as the changes in the size and/or composition of the vessels in response to dynamic and trophic stimuli. Inappropriate VR plays a crucial role in lumen loss and pathogenesis of cardiovascular diseases. Calcium channel blockers (CCBs) have been known to have vascular protective effects. However, the precise molecular mechanisms of these effects have not been fully elucidated. The aim of this study was to investigate the effects of nifedipine on intimal thickening and pathological VR, and to examine the role of the discoidin domain receptors (DDRs), which are collagen receptors, in the VR process in the collar model. Material and Methods: White rabbits were randomized into two groups. The groups received vehicle or nifedipine (40 mg/kg/day, p.o.) for three weeks. After seven days, a non-occlusive silicone collar was placed around the left carotid artery. To evaluate intimal thickening and VR, the intimal area, medial and luminal perimeters were measured. Furthermore, DDR expressions were assessed immunohistochemically. Results: Nifedipine did not inhibit intimal thickening. The collar provoked inward VR. Neither collagen content nor DDR expressions were affected by the collar. Nifedipine constituted hypertrophic outward expansive VR by involving luminal and arterial enlargement. However nifedipine did not change either collagen ingredient or DDR expressions. Conclusion: Nifedipine did not inhibit intimal thickening. However, it resulted in favorable expansive VR without changing collagen contents and DDR expressions. Thus, nifedipine may help to maintain luminal patency and to prevent restenosis after balloon angioplasty.