Suppression of experimental autoimmune uveoretinitis by prazosin, an alpha 1-adrenergic receptor antagonist

Curr Eye Res. 1992:11 Suppl:135-40. doi: 10.3109/02713689208999523.

Abstract

S-antigen (S-Ag)-induced experimental autoimmune uveoretinitis (EAU) was suppressed in Lewis and PVG rats by treatment beginning 4 days post immunization with prazosin, a specific alpha 1-adrenergic receptor antagonist. A significant suppression of EAU was observed at clinical and histological levels in both treated groups compared to a severe EAU which developed in controls. Fluorescein angiography showed no leakage of dye from the optic disc of a treated PVG rat presenting no ocular inflammation by clinical examination. The treatment had no effect on the titer of anti-S-Ag antibodies. Perivascular infiltrates of T-lymphocytes and macrophages together with alterations of blood-retinal barrier permeability are early events in EAU. Prazosin, by acting on the vascular alpha 1-adrenoreceptors, inhibits vasospasm, preserves blood-retinal-barrier integrity and prevents vascular edema and early inflammatory cell infiltration observed in EAU.

MeSH terms

  • Animals
  • Antigens
  • Arrestin
  • Autoantigens
  • Autoimmune Diseases / immunology*
  • Autoimmune Diseases / prevention & control
  • Capillary Permeability
  • Disease Models, Animal
  • Eye Proteins
  • Female
  • Fluorescein Angiography
  • Fundus Oculi
  • Immunosuppression Therapy
  • Prazosin / therapeutic use*
  • Rats
  • Rats, Inbred Lew
  • Retinal Vessels / pathology
  • Retinitis / immunology*
  • Retinitis / prevention & control
  • Uveitis / immunology*
  • Uveitis / prevention & control

Substances

  • Antigens
  • Arrestin
  • Autoantigens
  • Eye Proteins
  • Prazosin