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PETER R. LAIBSON, M.D.; NARENDRA KRISHNA, M.B.B.S., D.Sc. (Med.); IRVING H. LEOPOLD, M.D., D.Sc. (Med.)

Arch Ophthalmol. 1962;68(5):648-650.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Introduction

Sympathectomy as well as drugs, which block either the sympathetic nerve terminations or their effector sites, are known to lower intraocular pressure. With the availability of -methyl-dopa, it occurred to us to find out if a decarboxylase inhibitor would also produce the same effect.¹ -Methyl-dopa has been shown to prevent decarboxylation both in vitro and in vivo by the enzyme L-dopa decarboxylase, which catalyzes L-dopa to dopamine with the eventual formation of norepinephrine and epinephrine and L-5HTP to serotonin (Figs. 1 and 2).^2-4 The antidecarboxylase activity of -methyl-dopa, which thus results in the inhibition of subsequent biosynthesis of the sympathetic mediator levarterenol and serotonin, has been utilized with some success in the treatment of arterial hypertension and carcinoid tumor.^5-6 This approach of metabolic inhibition of catecholamines could throw some light on the somewhat controversial role assigned to epinephrine in the formation of aqueous humor, and perhaps . . . [Full Text PDF of this Article]

Author Affiliations
Philadelphia

From the Research Department of the Wills Eye Hospital.

Footnotes
Submitted for publication April 27, 1962.

Supported (in part) by grants from National Institute of Neurological Diseases and Blindness, National Institutes of Health, U.S. Public Health Service (Research Grant B-2555(R1) and National Council to Combat Blindness, Inc. (Grant-in-aid G-241) to Dr. Kirishna.

-Methyl-dopa (-methyl-3,4-dihydroxy-dl-phenylalanine; -methyl-3,4-dihydroxyphenylalanine; MK-350; methyl-dopa; Aldomet) used in this study was supplied by Merck Sharp & Dohme Research Laboratories, Division of Merck and Company, Inc., West Point, Pa.

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