Treatment of Ocular Hypertension by Adrenalin and Diverse Sympathomimetic Amines*

Weekers, R; Dflmarcelle, Y.; Gustin, Jillian

doi:10.1016/0002-9394(55)91493-8

Cited by 97 publications

(21 citation statements)

References 6 publications

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“…Before we address this latter question, a short digression to discuss another aspect of adrenergic influences on IOP is indicated. Although epinephrine, a mixed alpha and beta adrenergic agonist, was first used topically in the 1920's to treat glaucoma (17), it was Weekers (54) ~ho first demonstrated that isoproterenol, a beta adrenergic agonist, reduced pressure in the human eye. I_ater, Ross & Drance (41) showed the dose response relationship between isoproterenol and reduced IOP in humans.…”

Section: Methodsmentioning

confidence: 99%

A major pathway for the regulation of intraocular pressure

Sears

Mead

1983

Int Ophthalmol

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There has been a suspicion on the part of many clinicians and research scientists that intraocular pressure can be regulated by neural and/or humoral influences upon the rate of aqueous humor formation. It has been difficult, if not impossible, to separate specific influences of the central nervous system upon intraocular pressure from vascular induced or other secondary alterations. The past two decades have witnesses a great deal of study of the role of the adrenergic nervous system upon the regulation of intraocular pressure. From the investigations it is possible to formulate an integrated concept that can place years of work and speculation on a firm molecular foundation. The secretory tissue of the eye, the ciliary processes, contain an enzyme receptor complex, comprised by receptor complex, comprised by receptor bound membrane proteins, the catalytic moiety of the enzyme, a guanyl nucleotide regulatory protein (or N protein) and other features. The enzyme can be activated by well known neurohumoral or humoral agents that consist of catecholamines, glycoprotein hormones produced by the hypothalamic pituitary axis, and other related compounds, including placental gonadotropin. These compounds cause the ciliary epithelia to produce cyclic AMP at an accelerated rate. Cyclic AMP, as a second messenger, causes, either directly or indirectly, a decrease in the rate of aqueous humor formation that may be modulated by cofactors. Clinical syndromes fit the experimental data so that an integrated explanation can be given for the reduced intraocular pressure witnessed under certain central nervous system and adrenergic influences. The molecular biology of this concept provides important leads for future investigations that bear directly both upon the regulation of intraocular pressure and upon glaucoma.

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Section: Methodsmentioning

confidence: 99%

A major pathway for the regulation of intraocular pressure

Sears

Mead

1983

Int Ophthalmol

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“…The exact mechanism of the pressure-lowering effect of epinephrine is not fully understood. Based on evidence from fluorophotometry, tonography, and tonometry, epinephrine is believed to increase both conventional and unconventional outflow but certain observers found that uveoscleral outflow exceeded trabecular outflow (Weekers et al, 1955;Townsend and Brubaker, 1980;Schenker et al, 1981). Epinephrine may also stimulate aqueous humour production (Nagataki and Brubaker, 1981).…”

Section: Topical Adrenergic Agonistsmentioning

confidence: 99%

Pressure Lowering Medications

Tajudin¹,

Yaakub²

2011

Glaucoma - Current Clinical and Research Aspects

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“…However, the role of beta agonism leading to decreased aqueous production has still not been clarified. Isoproterenol, a potent beta stimulator, was first shown to reduce IOP by Weekers et al [1955]. The IOP reduction can be accounted for by a decrease in aqueous flow [Ross and Drance, 1970;Gaasterland et al, 19731. Epinephrine can be delivered as the hydrochloride, borate, or bitartrate salts.…”

Section: Adrenergic Agonistsmentioning

confidence: 99%

The pathogenesis and medical management of glaucoma

Caprioli

1985

Drug Development Research

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Caprioli, J.: The pathogenesis and medical management of glaucoma. Drug Dev. Res. 6~193-215, 1985. The term glaucoma applies to a group of diseases in which an elevated pressure in the eye causes optic nerve damage resulting in visual loss. Current medical and surgical treatment of glaucoma is designed to lower intraocular pressure to a level at which no further optic nerve damage occurs. This review serves to describe the following aspects of glaucoma and its treatment: aqueous humor dynamics and elevation of intraocular pressure; the pathogenesis of glaucomatous optic nerve damage; the nature of visual loss from glaucoma; the modern medical management of glaucoma; and a discussion of a new drug, forskolin, with potential for clinical use in the treatment of glaucoma.

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Treatment of Ocular Hypertension by Adrenalin and Diverse Sympathomimetic Amines*

Cited by 97 publications

References 6 publications

A major pathway for the regulation of intraocular pressure

A major pathway for the regulation of intraocular pressure

Pressure Lowering Medications

The pathogenesis and medical management of glaucoma

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