Study of pharmacological effects of nilvadipine on RCS rat retinal degeneration by microarray analysis

Sato, Motoya; Ohguro, Hiroshi; Ohguro, Ikuyo; Mamiya, Kazuhisa; Takano, Yoshiko; Yamazaki, Hitoshi; Metoki, Tomomi; Miyagawa, Yasuhiro; Ishikawa, Futoshi; Nakazawa, Makoto

doi:10.1016/s0006-291x(03)01092-1

Cited by 28 publications

(23 citation statements)

References 46 publications

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“…Despite these studies, however, Pawlyk et al [7] and Takano et al [12] did not find any rescue effects of D -cis-diltiazem on retinal degeneration in rd1 mice. Although the effects of D -cis-diltiazem on animal models of retinal degeneration remain controversial, we have previously shown that systemic administration of nilvadipine is effective for protecting photoreceptors in RCS rats [8,11], rd1 mice [12] and heterozygous rd2 mice [17]. However, the exact mechanisms of photoreceptor protection demonstrated by nilvadipine remain largely unknown.…”

Section: Discussionmentioning

confidence: 99%

“…However, the exact mechanisms of photoreceptor protection demonstrated by nilvadipine remain largely unknown. Besides possible roles of nilvadipine as a calcium channel blocker, expression of fibroblast growth factor-2 (FGF-2) is significantly increased following administration of nilvadipine in RCS rats and rd1 mice [11,12]. In addition, exogenous FGF-2 leads to photoreceptor protection in RCS rats [28], so nilvadipine, either directly or indirectly, seems likely to increase the expression of FGF-2 in the retina of these animal models.…”

Section: Discussionmentioning

confidence: 99%

“…Since intracellular concentrations of calcium ion were elevated in apoptosis [5], calcium channel blockers have been suggested as potential candidates to treat RP by protecting photoreceptors from apoptosis. Since Frasson et al [6] first reported the effects of D -cis-diltiazem, a calcium channel blocker, on photoreceptor protection in retinal degeneration 1 (rd1) mice, several investigators have reported positive and negative effects of calcium channel blockers on animal models of RP [7,8,9,10,11,12,13,14,15,16,17]. Nilvadipine is a derivative of dihydropyridine and has low-voltage-activated calcium blocking action in addition to the L -type high-voltage calcium-blocking action.…”

Section: Introductionmentioning

confidence: 99%

“…We speculated that nilvadipine might thus represent one of the best candidates to prevent photoreceptor apoptosis, penetrating the blood-retinal barrier more easily than other calcium blockers. We have already reported the protective effects of nilvadipine on photoreceptor degenerations in Royal College of Surgeons (RCS) rats, rd1 mice and rd2 (also called retinal degeneration slow, rds) mice [8,11,12,17]. Although these 3 different animal models of RP have been known to result from different genetic abnormalities [19,20,21], nilvadipine showed protective effects for each of these models.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Nilvadipine on Central Visual Field in Retinitis Pigmentosa: A 30-Month Clinical Trial

Nakazawa

Ohguro²,

Takeuchi³

et al. 2010

Ophthalmologica

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Purpose: To assess the effects of nilvadipine on the progression of central visual field defect in retinitis pigmentosa (RP). Design: Prospective, randomized, nonmasked, single-center trial. Methods: Patients with RP were randomly divided into a treated group receiving oral nilvadipine at 4 mg/day for ≧30 months and a control group receiving tocopherol nicotinate at 300 mg/day, helenien at 15 mg/day or no medication for the same periods. Progression of RP was evaluated using the 10-2 SITA Fast Program of the Humphrey Visual Field Analyzer, and regression coefficients calculated from the time courses of mean deviation (MD slope) were compared between groups. Results: Nineteen patients in the treated group and 14 patients in the control group completed the follow-up for ≧30 months. The mean (±standard deviation) duration of observation was 48.8 ± 11.8 months (median 48 months, range 30–66 months) for the treated group and 49.2 ± 18.1 months (median 48 months, range 30–90 months) for the control group (p = 0.94). Mean (±standard error of the mean, SEM) regression coefficients of the averaged MD values for the initial 30 months were –0.35 ± 0.17 dB/year in the treated group and –0.75 ± 0.06 dB/year in the control group (p < 0.01). Mean (±SEM) MD slopes for total observational periods were –0.49 ± 0.17 dB/year in the treated group and –0.89 ± 0.16 dB/year in the control group (mean ± SEM, p = 0.042). Conclusion: Nilvadipine at 4 mg/day significantly retarded progression of central visual field defects in RP in this small patient series.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effect of Nilvadipine on Central Visual Field in Retinitis Pigmentosa: A 30-Month Clinical Trial

Nakazawa

Ohguro²,

Takeuchi³

et al. 2010

Ophthalmologica

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“…They include treatments with steroids, 2-4 growth factors, 5 antioxidant combination therapy, 6,7 bile acids, 8 or calcium channel blockers. 9 A more recent approach, in which immune neuroprotective mechanisms are boosted, was shown to be effective also in a rat model of laser-induced retinal damage. 10,11 Preconditioning of the retina is a neuroprotective strategy based on the notion that a reversible injury of the retina makes it more resistant to further insults.…”

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confidence: 99%