The choroidal vasculature of the eye consists of a plexus of blood vessels located between the sclera and retina and provides blood flow critical for normal ocular function. In the present studies, I tested the hypothesis that autonomic nerves exert both acute and chronic influences on choroidal vascular function and structure in the adult rat. In the first aim, I characterized roles of autonomic nerves in short-term regulation of ocular blood flow. Sympathetic nerve stimulation elicited α1-adrenoreceptor mediated vasoconstriction in both the anterior and posterior choroid. Parasympathetic nerve stimulation produced nitric oxide-mediated vasodilation but only in the anterior choroid. Absence of posterior choroidal vasodilation was related to blunted guanylate cyclase responsiveness to nitric oxide.; In the second aim, I examined the role of nerves in long-term regulation of choroidal vasculature. Chronic sympathetic denervation resulted in substantial down-regulation of parasympathetic nitrergic vasodilation, but this was compensated for by increased muscarinic prejunctional autoreceptor facilitation, thus maintaining blood flow at normal levels.; Long-term sympathectomy also resulted in increased basal ocular blood flow. Structurally, the choroid was thicker and contained more venules and larger arterioles than control rats. Retinal capillary numbers were also increased in comparison with control choroid. Similar changes occurred following sympathetic deafferentation, suggesting that sympathetic nerve activity is required to maintain normal vascular architecture. Because similar changes occurred after chronic administration of the β-receptor antagonist propanolol, β-adrenoreceptors appear to play an important role in ocular angiostasis.; Possible roles of sensory or parasympathetic innervation were investigated following selective denervations. Neither sensory nor parasympathetic denervation alone altered choroidal vascularity. However, sensory nerve ablation significantly attenuated increased choroidal vascularity after sympathectomy, while parasympathetic denervation was without effect. Therefore, the post-sympathectomy increase in choroidal vascularity requires the presence of intact sensory innervation.; Together, these studies demonstrate that innervation not only regulates blood flow acutely, but also affects choroidal vascularity through sympathetic-sensory nerve interactions. Since peripheral nerve degeneration is a frequent complication of diabetes and aging, loss of innervation may contribute to the etiology of vascular retinopathies associated with these disorders.
展开▼
