Vein-to-artery graft surgery is used widely to by-pass arterial stenoses, but such grafts can fail over a prolonged period as a result of excessive neointimal hyperplasia causing thrombosis and graft occlusion. It has been suggested that neointimal hyperplasia, in vein grafts, is a result of the vessel wall adapting to the higher intraluminal pressure of the arterial circulation, compared with the venous circulation. Autologous artery grafts have been used to bypass arterial stenoses. Initially it was assumed that donor artery segments would not develop neointimal hyperplasia as they are already adapted to the arterial circulation but this is not so. In this study we postulated that surgical or postsurgical trauma was the cause of neointimal hyperplasia in autologous artery-to-artery grafts. In addition, as artery grafts are pre-adapted to the arterial circulation, autologous artery-to-artery grafts in hypertensive rats should develop similar levels of neointimal hyperplasia as seen in normotensive rats. Artery-to-artery grafts were placed in a series of 20 spontaneously hypertensive rats (SHR). In a separate series of sham grafting experiments the effects of anoxia and clamp trauma were assessed in SHR and WKy normotensive control rats. Finally, clamping, anoxia and anastomosis trauma were assessed in a similar series of rats. In the artery-to-artery graft series there was no difference in neointimal thickness between the SHR and that previously reported for normotensive rats. Minimal neointimal hyperplasia was demonstrated in the sham grafted series of rats and only slightly more in the single anastomosis series. It was only in the full grafting procedure that considerable neointimal hyperplasia developed. These data demonstrate that neointimal hyperplasia in artery-to-artery grafts is not exacerbated by the hypertension. In addition, trauma appears to be the initiator of neointimal hyperplasia and the extent of trauma correlates with the degree of neointimal hyperplasia.