Mechanisms of glomerular injury in experimental immune nephritis. II. Effect of a platelet activating factor receptor antagonist in an autologous nephritis model.
Arch Immunol Ther Exp (Warsz)
; 39(5-6): 575-86, 1991.
Article
en En
| MEDLINE
| ID: mdl-1668710
The role of Platelet Activating Factor (PAF) in experimental immune glomerulonephritis was assessed by administering the specific PAF receptor antagonist CV-3988 to inbred LEW rats with the Accelerated Autologous Nephrotoxic Serum Nephritis (AA-NTSN). Intravenous administration of CV-3988 caused a marked and sustained reduction in albuminuria and renal histopathological changes. Conversely, although CV-3988 appeared to modulate the fall in glomerular filtration rate (GFR) in the AA-NTSN, this trend was not statistically significant. Renal glomeruli isolated on day 1 after nephritis induction spontaneously released 16.9 +/- 2.2 ng of PAF per 200 glomeruli, while in glomeruli of healthy rats this secretion was virtually undetectable. The administration of CV-3988 to rats with AA-NTSN did not affect the following: binding of intravenously injected sheep anti-rat glomerular basement membrane (GBM) antibody; levels of autologous antibody to sheep immunoglobulin G; the functional integrity of circulating neutrophils. We conclude that local PAF generation and release is intimately linked with the pathogenesis of glomerular injury in this form of immune disease.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Glicoproteínas de Membrana Plaquetaria
/
Receptores de Superficie Celular
/
Receptores Acoplados a Proteínas G
/
Glomérulos Renales
/
Nefritis
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Arch Immunol Ther Exp (Warsz)
Año:
1991
Tipo del documento:
Article
País de afiliación:
Polonia
Pais de publicación:
Suiza