Nilvadipine Inhibits Acute Rise of Aqueous Flare and Intraocular Pressure Induced by Prostaglandin E&lt;sub&gt;2&lt;/sub&gt; in Pigmented Rabbits

Zhang, Xueyun; Hiraki, Shigeyoshi; Hayasaka, Seiji

doi:10.1159/000055467

Cited by 9 publications

(10 citation statements)

References 6 publications

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“…We therefore used pretreatment with nilvadipine, 100 Ìg/kg body weight, 30 min before PG administration in the present study. Our findings that pretreatment with nilvadipine inhibited the increased flare were quite similar to those reported by Zhang et al [5].…”

Section: Discussionsupporting

confidence: 93%

“…Zhang et al [5] previously reported that increased intracameral flare following PGE 2 administration was inhibited by nilvadipine in a dose-dependent manner (5-500 Ìg/kg Kadoi/Hiraki/Hayasaka/Ohtani body weight) and that nilvadipine injected 30 min before PG application suppressed the increase maximally. We therefore used pretreatment with nilvadipine, 100 Ìg/kg body weight, 30 min before PG administration in the present study.…”

Section: Discussionmentioning

confidence: 97%

“…Not all calcium channel blockers inhibit the acute rise of aqueous flare induced by PGE 2 in rabbits [3][4][5]. Chang et al [8] reported that nifedipine and nisoldipine (calcium channel blockers) inhibited the activity of phospholipase A 2 in a cell-free preparation of human platelets that acts on the release of arachidonic acid.…”

Section: Discussionmentioning

confidence: 99%

“…Nilvadipine, 5-isopropyl-3-methyl-2-cyano-1,4-dihydro-6-methyl-4-(m-nitrophenyl)-3,5-pyridinedicarboxylate, is another calcium channel blocker and is clinically used for the treatment of systemic hypertension. Zhang et al [5] reported that a small dose (5-500 Ìg/kg body weight) of nilvadipine inhibited the flare increase induced by PGE 2 . In the present study, we examined morphologically the disruption sites of the blood-aqueous barrier induced by PGE 2 in rabbit eyes pretreated with nilvadipine.…”

Section: Introductionmentioning

confidence: 99%

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Inhibitory Effect of Nilvadipine on Disruption of Blood-Aqueous Barrier Induced by Prostaglandin E2 Application in Pigmented Rabbits: A Morphologic Study

et al. 1999

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The purpose of the present study is to investigate the morphologic sites of breakdown in eyes pretreated with nilvadipine (a calcium channel blocker) that has been shown to inhibit the acute rise of aqueous flare induced by prostaglandin E₂ (PGE₂). Nilvadipine (100 µg/kg body weight) was injected intravenously in pigmented rabbits. Thirty minutes later, vehicle or PGE₂ (10, 50 or 250 µg/ml) was applied on the cornea by use of a glass cylinder. Forty-five minutes later, the animals received horseradish peroxidase (HRP) intravenously and the eyes were enucleated. Distribution of HRP in the anterior segments was observed by electron microscopy. Without nilvadipine pretreatment, HRP was seen in the intercellular space of nonpigmented cells of the eyes treated with 50 µg/ml PGE₂ and in the iris stroma of the eyes treated with 250 µg/ml PGE₂. With nilvadipine pretreatment, HRP was not observed in these sites. Our results indicate that nilvadipine suppresses disruption of the different sites of the blood-aqueous barrier.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Inhibitory Effect of Nilvadipine on Disruption of Blood-Aqueous Barrier Induced by Prostaglandin E2 Application in Pigmented Rabbits: A Morphologic Study

et al. 1999

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“…We have previously reported that PGE 2 -induced flare elevation was inhibited by nilvadipine and nicardipine (calcium channel blockers) [5,6]. Betaxolol is reported to have calcium-channel-blocking activity [7].…”

Section: Discussionmentioning

confidence: 99%

Effect of Topical Betaxolol on the Acute Rise of Aqueous Flare Induced by Highly Selective Agonists for Prostaglandin E2 Receptor Subtypes in Pigmented Rabbits

Yanagisawa¹,

Hayasaka²,

Zhang³

et al. 2002

Ophthalmic Res

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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 E₂ 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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Stability-indicating HPLC method for the determination of nicardipine in capsules and spiked human plasma. Identification of degradation products using HPLC/MS

Al-Ghannam

Al-Olayan

2019

Arabian Journal of Chemistry

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In this stability-indicating, reversed-phase high-performance liquid chromatographic method for nicardipine (NIC), forced degradation has been employed and the formed degradants were separated on a C18 (150 mm · 3.9 mm, 5 lm) analytical column using a mobile phase consisted of 70% methanol: acetic acid containing 0.01 M triethylamine with pH 4. The flow rate was 1.0 mL/min and the photodiode array detection wavelength was 353 nm. Forced degradation of the drug was carried out under acidic, basic, photolytic, and oxidative stress conditions. Chromatographic peak purity data indicated no co-eluting peaks with the main peaks. This method resulted in the detection of seven degradation products. Among these, two major degradation products from basic hydrolysis, one from oxidation by H 2 O 2 and four from photolytic stress were identified by mass spectral data. A good linear response was achieved over the range of 0.5-40 lg/mL with a limit of detection (LOD) of 0.011 lg/mL and limit of quantification (LOQ) of 0.036 lg/mL. The suggested method was successfully applied for the analysis of NIC in its commercial capsules, with mean% recovery value of 100.11 ± 2.26%. The method was extended to the in vitro determination on NIC in spiked human plasma samples with mean% recovery of 99.04 ± 5.67%. The suggested method was utilized to investigate the kinetics of photolytic induced degradation. ª 2014 The Authors. Production and hosting by Elsevier B.V. on behalf of King Saud University. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/).

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Nilvadipine Inhibits Acute Rise of Aqueous Flare and Intraocular Pressure Induced by Prostaglandin E<sub>2</sub> in Pigmented Rabbits

Cited by 9 publications

References 6 publications

Inhibitory Effect of Nilvadipine on Disruption of Blood-Aqueous Barrier Induced by Prostaglandin E<sub>2</sub> Application in Pigmented Rabbits: A Morphologic Study

Inhibitory Effect of Nilvadipine on Disruption of Blood-Aqueous Barrier Induced by Prostaglandin E<sub>2</sub> Application in Pigmented Rabbits: A Morphologic Study

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

Stability-indicating HPLC method for the determination of nicardipine in capsules and spiked human plasma. Identification of degradation products using HPLC/MS

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