Beta Adrenergic Binding Sites in the Human Eye: An Autoradiographic Study

Abstract

Beta adrenergic binding sites were localized and characterized in the human eye by means of "in vitro" autoradiography, using [125I] (-) iodocyanopindolol (125ICYP) as radioligand.Binding sites were visualized by apposition of isotope sensitive film to slide mounted eye sections. Receptor sites were present in the extraocular muscles, in the conjunctiva, in the epithelium and endothelium of the cornea, in the trabeculum and in the ciliary muscle. They were also present in the lens epithelium and in the retina. The pigmented ocular structures were heavily labelled but the binding was nonspecific. Characterization of these binding sites was achieved by testing the ability of selective adrenergic compounds to displace 125ICYP binding. These studies suggested that the majority of adrenergic binding sites in nonpigmented structures of human eye were of a beta2 type.

Effect of treatment by medicine or surgery on intraocular pressure and pulsatile ocular blood flow in normal-pressure glaucoma

“…We speculate that the negative effect of betaxolol on POBF may be due to an effect on cardiac output, for by inducing slower heart rate and reduction in myocardial contraction, the arterial flow to the upper body may be reduced, especially at night [11]. Previous reports have also suggested an increased vasoconstriction of the ocular vessels due to blockage of beta-receptors existing in the choroid, optic nerve head and retina [3,6]. Furthermore, the stimulation of alpha vascular receptors is not inhibited by the beta-blockers [7].…”

Effects of Atropine and Propranolol on Retinal Vessel Diameters during Isometric Exercise

“…The adrenergic system may, however, play a role in retinal blood flow regulation via humoral transmitters that may activate receptor sites located in retinal vessels. The presence of ß 1 -and ß 2 -adrenergic binding sites was proven in the retinal blood vessels promoting a relaxing response in smooth muscle cells [17,18].…”

Differential expression and role of hyperglycemia induced oxidative stress in epigenetic regulation of β1, β2 and β3-adrenergic receptors in retinal endothelial cells

“…However contrary to β1 and β2-adrenergic receptors, β3-adrenergic receptor couple through the inhibitory G protein (Gi), causing a reduced generation of cAMP [18]. Work in animal models suggests that adrenergic receptor agents may promote corneal wound healing and it is known that cornea has an abundance of β-adrenergic receptors in both the epithelium and endothelium of the cornea [19]. Previous studies demonstrate that β-adrenergic receptors agonists have positive effects on the retina by reducing the inflammatory markers [20-22].…”