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January 1987

β-Adrenergic Receptors in Human Trabecular Meshwork

Author Affiliations


Arch Ophthalmol. 1987;105(1):22. doi:10.1001/archopht.1987.01060010024007

To the Editor.  —We read with great interest the article by Drs Allen and Epstein1 demonstrating the additive effect of betaxolol and epinephrine in primary open angle glaucoma. They found that epinephrine increased outflow facility in the presence of betaxolol, but not in the presence of timolol. This led them to hypothesize that epinephrine increases outflow through a β2-adrenergic mechanism. We have recently demonstrated for the first time the presence of β-adrenergic receptors in human trabecular meshwork and in cultured trabecular cells.2 Furthermore, we determined that the vast majority of the β-adrenergic receptors were of the β2-adrenergic subtype. Our findings were subsequently confirmed by Kurtz et al3 using cultured human trabecular cells. These studies provide an anatomical basis for the concept that epinephrine acts through β2-adrenergic receptors in the trabecular meshwork to increase aqueous outflow facility.

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