Disease states characterized by ocular vascular pathology are often associated with impaired sympathetic function. This study examined the effect of sympathetic denervation on ocular vasculature of the adult rat. Uveal perfusion and choroidal and retinal blood vessel sizes and numbers were assessed in rats with intact innervation and after short- (2 days) or long-term (6 weeks) sympathetic denervation induced by ipsilateral superior cervical ganglion excision. In rats with intact innervation and after short-term sympathectomy, blood flow in both eyes was comparable. However, after long-term sympathectomy, blood flow was four-fold greater in the denervated than in the innervated eye, but was unaltered in lacrimal gland, cerebral cortex, and masseter muscle. Choroid surface area was not affected by long-term sympathectomy, but choroidal thickness was increased and choroidal cross-sectional area occupied by vascular lumina was greater. Arteriolar number per unit cross-sectional area of choroid was not altered although arteriolar diameters were enlarged. Choroidal venules were larger and more abundant. Choroidal capillary numbers were unchanged, but retinal capillaries of the outer plexiform layer were increased. To determine if these changes result from loss of sympathetic activity, sympathetic preganglionic innervation was excised chronically. This produced significant increases in choroidal thickness and vascular luminal area, and in numbers of arterioles, small venules, and capillaries in the outer plexiform layer. These findings show that sympathetic innervation is critical in regulating choroidal and retinal vascularity, and that chronic loss of sympathetic activity may contribute to abnormal vascular proliferation in diseases such as age-related macular degeneration and diabetic retinopathy.