Ocular Hypotensive Effects of Cholinergic and Adrenergic Drugs May be Influenced by Prostaglandins E2 in the Human and Rabbit Eye

Kaplan-Messas, Audrey; Naveh, Nava; Avni, Isaac; Marshall, Janene L.

doi:10.1177/112067210301300103

Cited by 14 publications

(6 citation statements)

References 12 publications

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“…In addition to reports describing the use of PGF 2a related drugs, 1-3 8-10 the relation between glaucoma ophthalmic solutions and endogenous PGs has also been described in other reports, including that by Kaplan-Messas et al, 17 who reported that endogenous PGE 2 is produced in isolated human iris upon administration of ophthalmic solution containing 2% pilocarpine and 1% adrenaline (epinephrine). In addition to the report by Yousufzai et al, 7 which described the release of endogenous PGE 2 , PGD 2 , PGF 2a , and arachidonic acid (AA), there are some reports describing the release of PGE 2 .…”

Section: Discussionmentioning

confidence: 88%

Effect of non-steroidal anti-inflammatory ophthalmic solution on intraocular pressure reduction by latanoprost in patients with primary open angle glaucoma or ocular hypertension

Chiba

Kashiwagi²,

Chiba³

et al. 2006

British Journal of Ophthalmology

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Aim: To investigate the effects of a non-steroidal anti-inflammatory drug (NSAID) ophthalmic solution on latanoprost induced intraocular pressure (IOP) reduction in glaucoma patients. Methods: Examination was conducted on 16 eyes of 16 glaucoma patients who had been given only latanoprost for at least 6 weeks. The NSAID ophthalmic solution, sodium 2-amino-3-(4-bromobenzoyl) phenylacetate sesquihydrate, was additionally given for 12 weeks into one eye (NSAID group), while sodium hyaluronic acid ophthalmic solution was administered into the other eye (control group) in a double masked fashion. The IOP measurement was performed before the start of additional administration of ophthalmic solutions, 2, 4, 6, 8, 10, and 12 weeks after the start of additional administration, and 2, 4, and 6 weeks after discontinuing additional administration. Results: No significant difference was observed in the IOPs before additional administration of ophthalmic solution between the NSAID group and the control group. Following the additional administration of ophthalmic solution, IOP in the NSAID group was consistently higher than that in the control group, and a maximum difference in IOP between the two groups was 1.08 (SD 1.75) mm Hg (p = 0.03). This trend was observed even after additional administration was discontinued. Conclusion: NSAID ophthalmic solution may partly affect IOP reduction by latanoprost. L atanoprost is a phenyl substituted analogue of prostaglandin F2a (PGF 2a ), and is widely used for the treatment of glaucoma because of its excellent potent intraocular pressure (IOP) reduction. 1-3Although the mechanism of IOP reduction by latanoprost is thought to increase the uveoscleral outflow as a result of remodelling the extracellular matrix of ciliary muscle mediated by FP receptors, the details of this mechanism remain unclear.1 4-6 PGF 2a related drugs have been reported to produce endogenous prostaglandins (PGs), and several reports have suggested that induction of endogenous PGs is involved in IOP reduction. [7][8][9] Although it appears certain that endogenous PGs are produced by administering PGF 2a related drugs based on the results of basic experiments, 7 8 since the action of PG on the eyes shows species differences, the results of basic and animal experiments cannot be directly applied to the human eye.2 Therefore, we have conducted a study on the action of endogenous PGs on IOP resulting from the administration of PGF 2a in healthy volunteers, and found that the IOP reduction of latanoprost is inhibited by the administration of NSAID ophthalmic solution.10 However, there have yet to be studies on the effect of NSAID ophthalmic solution on the IOP reduction of latanoprost in glaucomatous human eyes.In this study, a prospective double blind study was conducted to assess the effect of administering NSAID ophthalmic solution on the IOP reduction of latanoprost, targeting patients with primary open angle glaucoma (POAG) or ocular hypertension (OH). SUBJECTS AND METHODSAll experiments were conducted in accordance...

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Section: Discussionmentioning

confidence: 88%

Effect of non-steroidal anti-inflammatory ophthalmic solution on intraocular pressure reduction by latanoprost in patients with primary open angle glaucoma or ocular hypertension

Chiba

Kashiwagi²,

Chiba³

et al. 2006

British Journal of Ophthalmology

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“…Indeed, COX-2, prostaglandin E(2) and EP2 receptor activity have been identified in cells of the human ciliary body (Liang et al, 2003, 2004; Rosch et al, 2005) perhaps accounting for the ability of Butaprost™ (an EP2 agonist) to lower IOP. Of great interest is that cholinergic and adrenergic anti-glaucoma drugs induce the production of PGE2 in vitro from the iris-ciliary body of rabbits and irises of glaucoma patients (Kaplan-Messas et al, 2003), perhaps accounting, in part, for the hypotensive effects of pilocarpine and epinephrine on IOP. Furthermore, COX-2 expression is virtually absent in the NPE cells in patients with primary open-angle glaucoma (Maihöfner et al, 2001).…”

Section: Cannabinoids and Ocular Tissuesmentioning

confidence: 99%

Endocannabinoids in the retina: From marijuana to neuroprotection

Yazulla¹

2008

Progress in Retinal and Eye Research

148

143

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The active component of the marijuana plant Cannabis sativa, Δ 9 -tetrahydrocannabinol (THC), produces numerous beneficial effects, including analgesia, appetite stimulation and nausea reduction, in addition to its psychotropic effects. THC mimics the action of endogenous fatty acid derivatives, referred to as endocannabinoids. The effects of THC and the endocannabinoids are mediated largely by metabotropic receptors that are distributed throughout the nervous and peripheral organ systems. There is great interest in endocannabinoids for their role in neuroplasticity as well as for therapeutic use in numerous conditions, including pain, stroke, cancer, obesity, osteoporosis, fertility, neurodegenerative diseases, multiple sclerosis, glaucoma and inflammatory diseases, among others. However, there has been relatively far less research on this topic in the eye and retina compared with the brain and other organ systems. The purpose of this review is to introduce the "cannabinergic" field to the retinal community. All of the fundamental work on cannabinoids has been performed in non-retinal preparations, necessitating extensive dependence on this literature for background. Happily, the retinal cannabinoid system has much in common with other regions of the central nervous system. For example, there is general agreement that cannabinoids suppress dopamine release and presynaptically reduce transmitter release from cones and bipolar cells. How these effects relate to light and dark adaptation, receptive field formation, temporal properties of ganglion cells or visual perception are unknown. The presence of multiple endocannabinoids, degradative enzymes with their bioactive metabolites, and receptors provides a broad spectrum of opportunities for basic research and to identify targets for therapeutic application to retinal diseases.

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“…8 reported that coadministration of a nonsteroidal anti-inflammatory drug (NSAID) inhibits latanoprost-induced IOP reduction in normal volunteers. Kaplan-Messas et al 9 indicated that cholinergic and adrenergic drug-induced endogenous PGE2 production in the iris-ciliary body may have a role in the hypotensive effect of adrenergic and cholinergic drugs. 9 These reports suggest that not only the administered drug but also PG produces endogenously after drug application and non-FP prostanoid receptors may contribute to PG analogue-induced reduction of IOP.…”

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confidence: 99%

The Effects of Prostaglandin Analogues on Prostanoid EP1, EP2, and EP3 Receptor-Deficient Mice

Ota

Aihara

Saeki

et al. 2006

Invest. Ophthalmol. Vis. Sci.

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Ocular Hypotensive Effects of Cholinergic and Adrenergic Drugs May be Influenced by Prostaglandins E2 in the Human and Rabbit Eye

Abstract: The study found an increase in in vitro production of PGE2 by the irises of eyes treated with cholinergic and adrenergic antiglaucoma medications. This suggests a role for endogenous PG production in the hypotensive effect of both classes of drug.

Cited by 14 publications

References 12 publications

Effect of non-steroidal anti-inflammatory ophthalmic solution on intraocular pressure reduction by latanoprost in patients with primary open angle glaucoma or ocular hypertension

Effect of non-steroidal anti-inflammatory ophthalmic solution on intraocular pressure reduction by latanoprost in patients with primary open angle glaucoma or ocular hypertension

Endocannabinoids in the retina: From marijuana to neuroprotection

The Effects of Prostaglandin Analogues on Prostanoid EP1, EP2, and EP3 Receptor-Deficient Mice

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