Persistence on prostaglandin ocular hypotensive therapy: an assessment using medication possession and days covered on therapy. (33/104)

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Prostaglandin E2 receptor subtype EP2- and EP4-regulated gene expression profiling in human ciliary smooth muscle cells. (34/104)

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Smooth muscle proliferation and role of the prostacyclin (IP) receptor in idiopathic pulmonary arterial hypertension. (35/104)

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Treatment of pulmonary arterial hypertension: the role of prostacyclin and prostaglandin analogs. (36/104)

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Intraocular pressure changes in the contralateral eye after topical treatment: does an "ophthalmotonic consensual reaction" exist? (37/104)

BACKGROUND: The existence of "ophthalmotonic consensual reaction," a contralateral change in intraocular pressure in the fellow eye induced by treatment of the first eye only, was suggested in 1924. Since then, the validity of this mechanism has been controversial. OBJECTIVES: To assess intraocular pressure changes in the contralateral fellow eyes of patients treated with IOP-lowering medication in one eye, and investigate the existence of an ophthalmotonic consensual reaction. METHODS: The study population included 38 patients with newly diagnosed bilateral ocular hypertension or early open angle glaucoma. One eye of each patient was randomly treated with one of five compounds: prostaglandin analogues, beta-blockers, alpha-2 agonists, carbonic anhidrase inhibitors and a combination therapy: dorzolamide hydrochloride-timolol maleate (Cosopt, Merck Sharpe & Dohme). The eye with the higher baseline IOP was selected to be the treated eye. After 3 weeks a masked examiner measured the IOP in both the treated and untreated eye. RESULTS: Mean IOP of the treated eyes at baseline was 26.1 +/- 4.2 mmHg and at follow-up 20.2 +/-2.9 mmHg, a reduction of IOP from baseline of -6 +/- 3.8 mmHg, a mean percent reduction of -22 +/- 10.1%. In the contralateral eyes, the mean IOP at baseline was 24.2 +/- 3 mmHg and 23.1 +/- 3.1 mmHg at follow-up; IOP reduction from baseline was -1.2 +/- 1.8 mmHg, or mean percent reduction -4.7 +/- 7.1%. A major contralateral IOP decrease was seen only in the beta-blockers and the combination (Cosopt) treatment groups (-6.1 +/- 8.3% and -12.3 +/- 8.3% mean percent reduction, respectively, P < 0.05). The contralateral eyes in the prostaglandin analogues, CAI or alpha2-agonist groups showed only a small change in IOP (-2.6 +/- 4.6%, -3.2 +/- 2.6%, +0.7 +/- 3.3%, mean percent reduction, respectively, P < 0.05). CONCLUSIONS: The existence of an ophthalmotonic consensual reaction was not supported.  (+info)

Prostaglandin receptors on human platelets. Structure-activity relationships of stimulatory prostaglandins. (38/104)

1. Synthetic analogues of prostaglandins E2 or F2a (monocyclic bisenoic prostaglandins), like the endogenous prostaglandin endoperoxides (prostaglandins G2 and H2) from platelets, and like synthetic analogues of prostaglandin H2 (bicyclic bisenoic prostaglandins), can induce aggregation of human platelets, although prostaglandins E2 and F2a themselves are inactive. 2. All the prostanoid compounds that induce platelet aggregation release 5-hydroxytryptamine from platelet dense bodies, but do not release beta-N-acetylglucosaminidase from lysosomal granules. Arachidonic acid evokes a similar response. 3. All endoperoxide analogues tested (bicyclic compounds) were powerful platelet stimulants, and all active compounds (whether mono- or bi-cyclid) apparently acted via the same receptor as the endogenous prostaglandin endoperoxides. 4. The nature and stereospecificity of substituents at positions 11 and 15 (or 16) on prostaglandin E2 are critical determinants for platelet-stimulating activity: deoxy substitution at position 11 plus methylation at position 15 (or 16) produces a potent stimulant, particularly if the groups around C-15 are in the S configuration. 5. The effects of these structural modifications are apparently due to, at least in part, a change in side-chain conformation.  (+info)

Incidence of new coding for dry eye and ocular infection in open-angle glaucoma and ocular hypertension patients treated with prostaglandin analogs: retrospective analysis of three medical/pharmacy claims databases. (39/104)

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EP3, but not EP2, FP, or TP prostanoid-receptor stimulation may reduce intraocular pressure. (40/104)

Stimulation of DP, but not TP or FP, prostanoid receptors has previously been shown to reduce intraocular pressure (IOP) in rabbits. However the role of EP receptors (EP1, EP2, and EP3 subtypes) has not been studied extensively. Sulprostone, RS-61565, and RS-20216 have been studied for effects on rabbit IOP, and their prostanoid-receptor profiles characterized. The data suggest that the EP3, but not EP2, FP, or TP activity of these agonists correlated with the intraocular hypotensive effects. Moreover, RS-20216 lowered IOP at a dose of 5 micrograms for up to 12 hr after administration. In contrast to PGE1 and PGE2, which elicited both hyper- and hypotensive responses, sulprostone, RS-61565, and RS-20216 elicited only a hypotensive responses with no signs of ocular irritation. Thus stimulation of the EP3 receptor results in a lowering of IOP in rabbits. Compounds specific for this receptor subtype may act as novel therapeutic agents for the treatment of glaucoma.  (+info)