A model is proposed for initiation and inhibition of growth in retinal vessels including the control of proliferative diabetic retinopathy by photocoagulation. The model assumes that chronic dilatation (constriction) of a retinal blood vessel causes (inhibits) growth. Destruction of rods and cones by photocoagulation allows more choroidal oxygen to reach the inner retina and constrict retinal vessels. The attenuated vessels in late stage retinitis pigmentosa are an analogous and exaggerated effect to that from photocoagulation. The control of proliferative diabetic retinopathy is compared to the cause of retrolental fibroplasma. Following vitrectomy the retina utilizes oxygen from the aqueous which results in dilatation of iris vessels followed by rubeosis iridis. From this model, neovascularization from the disc or angle vessels follows the dilatation resulting from increased flow in their distal vascular beds.