title: Preservation of retinal morphology and functions in royal college surgeons rat by nilvadipine, a Ca(2+) antagonist.
abstract: OBJECTIVE
  The Royal College of Surgeons (RCS) rat is the most extensively studied animal model for understanding the molecular pathology in inherited retinal degeneration, such as retinitis pigmentosa (RP). The purpose of the present study was to evaluate the pharmacologic effects of several Ca(2+) antagonists on the retinal degeneration of RCS rats.
  
  
  METHODS
  Several Ca(2+) antagonists, diltiazem, nicardipine, nilvadipine, and nifedipine, were intraperitoneally administered and retinal morphology and functions analyzed.
  
  
  RESULTS
  Among the Ca(2+) antagonists, only intraperitoneally administered nilvadipine preserved retinal morphology and electroretinogram responses in RCS rats during the initial stage of retinal degeneration. Studies using immunohistochemistry, RT-PCR, and Western blot analysis revealed significant enhancement of rhodopsin kinase and alphaA-crystallin expression and suppression of caspase 1 and 2 expression in the retina of nilvadipine-treated rats.
  
  
  CONCLUSIONS
  These data suggest that nilvadipine is beneficial for the preservation of photoreceptor cells in RCS rats and can be used to treat some patients with RP.
authors.affiliation: Department of Ophthalmology, Hirosaki University School of Medicine, Hirosaki, Japan.
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Yamazaki
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ohguro
authors.forename: Tadao
authors.initials: T
authors.lastname: Maeda
authors.forename: Ikuyo
authors.initials: I
authors.lastname: Maruyama
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Takano
authors.forename: Tomomi
authors.initials: T
authors.lastname: Metoki
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Nakazawa
authors.forename: Hajime
authors.initials: H
authors.lastname: Sawada
authors.forename: Mari
authors.initials: M
authors.lastname: Dezawa
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D020170:Caspase 1 / Q000235:genetics / Q000378:metabolism; D053143:Caspase 2; D020169:Caspases / Q000235:genetics / Q000378:metabolism; D003459:Crystallins / Q000235:genetics / Q000378:metabolism; D017931:DNA Primers / Q000737:chemistry; D004195:Disease Models, Animal; D004591:Electrophoresis, Polyacrylamide Gel; D004596:Electroretinography; D005136:Eye Proteins; D019084:Fluorescent Antibody Technique, Indirect; D051606:G-Protein-Coupled Receptor Kinase 1; D007274:Injections, Intraperitoneal; D009543:Nifedipine / Q000031:analogs & derivatives* / Q000494:pharmacology*; D011494:Protein Kinases / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011922:Rats, Mutant Strains; D012160:Retina / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology / Q000648:ultrastructure; D012174:Retinitis Pigmentosa / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D002121:Calcium Channel Blockers; D003459:Crystallins; D017931:DNA Primers; D005136:Eye Proteins; D012333:RNA, Messenger; C035100:nilvadipine; D011494:Protein Kinases; D051606:G-Protein-Coupled Receptor Kinase 1; C496765:Grk1 protein, rat; D053143:Caspase 2; D020169:Caspases; D020170:Caspase 1; D009543:Nifedipine