Beta-adrenergic receptors in human anterior optic nerve: An autoradiographic study

Abstract

SUMMARYSections of human anterior optic nerve and nerve head were incubated in a physiological solution containing a radiolabelled beta blocker at a low concentration. Tbe beta blocker used was (-)-e25iodo )-cyanopindolol, which has a higb affinity and specificity for beta-adrenergic receptors. Concurrent incubations were performed with a great excess of unlabelled beta blocker added to demon strate non-specific binding. Following incubation the sec tions were washed and dried. Tbey were then apposed to photographic film for 5 days and developed. Incubations were performed witb the stereoisomers of propranolol and an alpha blocker as well as specific beta-one and beta-two blockers. Beta-adrenergic receptors were demonstrated in anterior optic nerve and optic nerve head. The majority were of the beta-two subtype.

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].…”

Decrease of optic disc cupping and pallor of ocular hypertensives with timolol therapy

“…However, Yoshida et al [32] have noted in young normals a significant mean decrease of 3% in diameter of the retinal arteries 90 minutes after the application of timolol drops compared to placebo drops. Also beta adrenergic receptors have been identified in the human anterior optic nerve [33] as well as human retinal blood vessels (341. This suggests that a possible mechanism for the effect of timolol on reversing optic disc parameters is to increase blood flow.…”

Secondary neuroprotective effects of hypotensive drugs and potential mechanisms of action

“…The β-adrenoreceptor receptors are localized to the ciliary epithelium and vascular smooth muscle, so β-blockers are intimately involved not only in the mediation of aqueous humor production, but also smooth muscle relaxation. While β-receptors have long been known to localize to both retinal arteries and veins [87], β-adrenergic binding sites also localize to vessel-free areas of the neural retina and optic nerve [77,88,89]. Blockers such as betaxolol have been demonstrated to increase blood velocity in the human ONH, thus supporting the hypothesis that mediation of vasculature effects may temper ischemia-induced RGC injury [90].…”

“…Their hypotensive effect is primarily mediated by the decrease of aqueous fluid with antagonism of β-adrenoreceptors in the anterior chamber of the eye [77,78]. Multiple studies have demonstrated evidence for a secondary neuroprotective effect of this class of drugs.…”