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Maurice E. Langham, PhD
Baltimore

Arch Ophthalmol. 1970;84(2):237.

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

To the Editor.

—At the science writers seminar in Los Angeles from Nov 8 through Nov 11 which was organized by Research to Prevent Blindness, I had been invited to review our recent research on the role of adrenergic mechanisms in the regulation of intraocular pressure and to assess the contribution of our findings to new therapeutic approaches in the treatment of glaucoma. In the period of open discussion during the seminar, great interest was shown in the possibility of immediate and widespread application to our findings.

The experimental basis for this new therapeutic approach has been reported in recent publications.^1-3 The results showed that pupil dilatation and decreased intraocular pressure induced by topically applied norepinephrine could be increased in both magnitude and duration by the application of a compound which inhibited the uptake of norepinephrine into the adrenergic neurone. In addition, adrenergic potentiators alone caused pupil dilatation . . . [Full Text PDF of this Article]

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