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      Effect of Topical Betaxolol on the Acute Rise of Aqueous Flare Induced by Highly Selective Agonists for Prostaglandin E 2 Receptor Subtypes in Pigmented Rabbits

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          Purpose: To evaluate the role of topical betaxolol on experimental ocular inflammation in rabbits. Method: Transcorneal diffusion of highly selective agonists for prostaglandin E<sub>2</sub> receptor subtypes (EP), 25 µg/ml, with the use of a glass cylinder, was performed to produce aqueous flare elevation in pigmented rabbits. Betaxolol was topically administered before EP agonist application. Aqueous flare was measured with a laser flare cell meter. Results: Performing topical instillation of 0.5% betaxolol 4 times inhibited 52 ± 9% of EP2-agonist (ONO-AE1-259-01)-induced aqueous flare elevation. The inhibition of flare elevation was dependent on the number of betaxolol instillations. Betaxolol did not suppress the elevation induced by an EP4 agonist (ONO-AE1-392). Conclusion: Betaxolol inhibited EP2-agonist-induced aqueous flare elevation in pigmented rabbits.

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          Ca2+ channel-blocking activity of propranolol and betaxolol in isolated bovine retinal microartery.

           Eric Hoste,  S Sys (1998)
          The relaxant action of the standard beta-blocker propranolol was compared with betaxolol, a beta-blocker with established vasorelaxant properties. Ring segments of bovine retinal microartery (n=36, theta=237 microm), which lacks adrenergic nerves and beta-adrenoceptors, were mounted in an organ bath for isometric force recording. l-, d-, dl-Propranolol and betaxolol were equally effective in relaxing tonic K+-induced contractions. The median effective dose (ED50) value was approximately 10(-5) M for both beta-blockers. The relaxation by both beta-blockers was unaffected by endothelium removal. Like verapamil, both beta-blockers induced smaller relaxation of tonic prostaglandin F2alpha (PGF2alpha)-induced force, which depended less on Ca2+ influx than did K+-induced force: K+-, but not PGF2alpha-induced contractions were abolished in Ca2+-free medium. The minor betaxolol-induced relaxation of tonic PGF2alpha-induced force was blocked in Ca2+-free medium. With repeated exposures to PGF2alpha in Ca2+-free medium, initial phasic PGF2alpha-induced force declined less with every exposure than did subsequent tonic force. When the preparations were briefly equilibrated with K+- and Ca2+-rich solution before every exposure to PGF2alpha phasic force did not decline, indicating that phasic force primarily depended on Ca2+ released from intracellular stores. Both beta-blockers failed to relax phasic PGF2alpha-induced force. Thus propranolol and betaxolol are equipotent vasorelaxant drugs in retinal microartery, both probably acting via Ca2+ channel blockade. This activity (that shows no stereospecificity) thus appears to be a more general property of beta-blockers. Microarteries might be more sensitive to this activity than are conductance arteries.
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            Nilvadipine Inhibits Acute Rise of Aqueous Flare and Intraocular Pressure Induced by Prostaglandin E 2 in Pigmented Rabbits

            To evaluate the possible role of calcium channel blocker on changes in aqueous flare and intraocular pressure induced by prostaglandin E 2 (PGE 2 ) in pigmented rabbits, we examined the effects of nilvadipine and nicardipine (calcium channel blockers). PGE 2 , 25 µg/ml, was administered using a glass cylinder. Nilvadipine or nicardipine was injected intravenously. Aqueous flare was measured by a laser flare cell meter. Intraocular pressure was measured by a noncontact tonometer. After administration of PGE 2 , aqueous flare and intraocular pressure increased and then decreased. Increased flare and elevated intraocular pressure following PGE 2 administration were inhibited by nilvadipine in a dose-dependent manner (5–500 µg/kg body weight). These responses were inhibited only slightly by nicardipine at the same concentration. Nilvadipine injected 30 min before PGE 2 application inhibited the increase maximally. The inhibitory effect was found on days 1, 3, 5, and 7 by daily administration of nilvadipine. A good correlation between the inhibition of intraocular pressure and the inhibition of increased flare by nilvadipine was found. We believe that Ca 2+ , or calcium channel blocker-related substances may be involved in the mechanism of PGE 2 -induced elevation of aqueous flare and intraocular pressure in the pigmented rabbit.
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              Effects of Nilvadipine, Nicardipine and Verapamil on Acute Rise of Aqueous Flare Induced by Iris Photocoagulation or Intravenous Lipopolysaccharides in Pigmented Rabbits

              The effects of nilvadipine, nicardipine and verapamil on the acute rise of aqueous flare induced by argon laser photocoagulation of the iris or by intravenous injection of lipopolysaccharides (LPS, 0.5 µg/kg) were investigated in pigmented rabbits. Nilvadipine, nicardipine and verapamil were injected intravenously. Aqueous flare was measured with a laser flare cell meter. Following photocoagulation, aqueous flare increased, reached its maximum at 45–75 min and then decreased. After administration of LPS, aqueous flare increased, reached its maximum at 4 h and then returned to baseline levels at about 24 h. Flare reactions were inhibited by nilvadipine in a dose-dependent manner. The elevations were maximally inhibited by nilvadipine 30 min before photocoagulation or intravenous LPS. Two hundred micrograms per kilogram of nilvadipine inhibited 81% of photocoagulation-induced flare elevation, while the same dose of nicardipine and verapamil inhibited 19 and 9% of the elevation, respectively. The same dose of nilvadipine inhibited 51% of LPS-induced flare elevation, while the same dose of nicardipine and verapamil inhibited 6 and 4% of the elevation, respectively. In conclusion, nilvadipine inhibited the experimental elevation of aqueous flare more effectively than did nicardipine and verapamil.

                Author and article information

                Ophthalmic Res
                Ophthalmic Research
                S. Karger AG
                February 2002
                07 February 2002
                : 34
                : 1
                : 48-50
                Department of Ophthalmology, Toyama Medical and Pharmaceutical University, Toyama, Japan
                48325 Ophthalmic Res 2002;34:48–50
                © 2002 S. Karger AG, Basel

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                Page count
                Figures: 3, References: 7, Pages: 3
                Original Paper

                Vision sciences, Ophthalmology & Optometry, Pathology

                Betaxolol, Aqueous flare, EP4 agonist, EP2 agonist


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