Increased Plasma Free Cortisol in Ocular Hypertension and Open Angle Glaucoma

Schwartz, Bernard; McCarty, George R.; Rosner, Bernard

doi:10.1001/archopht.1987.01060080062029

Cited by 49 publications

(20 citation statements)

References 13 publications

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“…It has been well documented that glucocor ticoids increase ocular pressure in pharmaco logic doses and are associated at physiologic and supraphysiologic ranges with increased ocular pressure in both glaucoma and ocular hypertension [9]. However, the role of minerMineralocorticoid Receptors in the Ophthalmic Res 1997;29:42-47 alocorticoids in the control of ocular pressure is less clear.…”

Section: Discussionsupporting

confidence: 42%

Mineralocorticoid Receptors in the Rabbit Iris-Ciliary Body

Schwartz¹,

Wysocki²

1997

Ophthalmic Res

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To demonstrate the presence of mineralocorticoid receptors, specifically aldosterone receptors, iris-ciliary body cytosol from New Zealand albino rabbits was incubated with increasing amounts (0.5–20.0 nM) of radiolabeled aldosterone in the presence and absence of a 100-fold excess of aldosterone. A glucocorticoid receptor blocker, RU-28362, was employed when various steroids were allowed to compete with aldosterone for binding sites on the aldosterone receptor. Aldosterone bound to two classes of receptor proteins. Scatchard analysis of the data indicated one component to bind aldosterone with high affinity (K_d = 2.2 × 10^––9M) and low capacity (B_max = 32 fmol/mg protein). If the concentration of aldosterone is increased, it also binds to a second component, but with a lower affinity (K_d = 9.8 × 10^––9M) and greater capacity (B_max = 64 fmol/mg protein).

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Section: Discussionsupporting

confidence: 42%

Mineralocorticoid Receptors in the Rabbit Iris-Ciliary Body

Schwartz¹,

Wysocki²

1997

Ophthalmic Res

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“…The rationale is that since glucocorticoids raise human intra-ocular pressure, especially in patients with open-angle glaucoma, a pe ripheral glucocorticoid blocker should lower it, especially if such patients have raised free plasma cortisol [8],…”

Section: Discussionsupporting

confidence: 41%

Topical Dexamethasone Lowers Rabbit Ocular Tension, as Does Topical Mifepristone (RU 486), a Peripheral Blocker of Dexamethasone and Progesterone

Phillips

Peat²,

Gore³

et al. 1989

Ophthalmic Res

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The variability of the response of the rabbit eye to topical 1 % dexamethasone has been shown in two groups of 20 young albino rabbits each (total 40) tested in succession. The pressure anomalously fell significantly (but by only 1 mm Hg) in both groups in the first 4 weeks of administration, but not in subsequent weeks. Mifepristone (RU 486), a peripheral antagonist of dexamethasone and progesterone, reduced the pressure significantly, again by only 1 mm Hg, in the first group of 20 rabbits, not the second. Accordingly, no conclusion was possible on the originating question: does pre-treatment with mifepristone prevent the dexamethasone-induced rise in rabbit intra-ocular pressure?

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“…Studies show that approximately 90% of patients with POAG experienced an IOP elevation greater than 6 mm Hg after receiving topical 0.1% dexamethasone for 4 weeks (Armaly, 1963). In addition, studies demonstrate that POAG patients have elevated levels of the endogenous glucocorticoid, cortisol, in their serum as well as in the aqueous humor compared to age-matched subjects without POAG (Ray et al, 1977;Rozsival et al, 1981;Schwartz et al, 1987).…”

Section: Introductionsupporting

confidence: 39%

The Effects of Glucocorticoids on Trabecular Meshwork and its Role in Glaucoma

Genis¹

2015

American Journal of Biochemistry and Biotechnology

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Primary Open-Angle Glaucoma (POAG), an optic neuropathy that is a leading cause of irreversible blindness, has been studied extensively in hopes of better understanding its underlying mechanism. Glucocorticoids (GC) are commonly used to treat inflammatory ocular conditions but are also known to increase the risk of glaucoma by raising Intraocular Pressure (IOP) in susceptible individuals, leading to steroidinduced glaucoma. Based on clinical studies as well as molecular experiments, steroid-induced glaucoma and POAG show many similarities, including a common underlying mechanism of IOP elevation. Studying steroid-induced glaucoma can reveal more about the pathways underlying decreased outflow of aqueous humor and POAG. GCs have been shown to cause numerous structural changes in the Trabecular Meshwork (TM), including thickening of trabecular beams, activation of TM cells and increased deposition of extracellular material. GCs also upregulate the expression of MYOC (myocilin) in human TM, a gene whose mutation is linked to 10% of juvenile glaucoma cases. Other studies demonstrate that GCs downregulate PLAT, which codes for tissue Plasminogen Activator (tPA) and decrease Matrix Metalloproteinase (MMP) gene expression. In addition, tPA administration has been shown to prevent GC-induced IOP elevation in sheep eyes. The present review demonstrates some of the important interactions between GCs and the TM that can lead to novel therapeutic measures in the setting of steroidinduced glaucoma as well as POAG.

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Increased Plasma Free Cortisol in Ocular Hypertension and Open Angle Glaucoma

Cited by 49 publications

References 13 publications

Mineralocorticoid Receptors in the Rabbit Iris-Ciliary Body

Mineralocorticoid Receptors in the Rabbit Iris-Ciliary Body

Topical Dexamethasone Lowers Rabbit Ocular Tension, as Does Topical Mifepristone (RU 486), a Peripheral Blocker of Dexamethasone and Progesterone

The Effects of Glucocorticoids on Trabecular Meshwork and its Role in Glaucoma

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