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Titolo:
ARGININE METABOLISM IN EXPERIMENTAL GLOMERULONEPHRITIS - INTERACTION BETWEEN NITRIC-OXIDE SYNTHASE AND ARGINASE
Autore:
COOK HT; JANSEN A; LEWIS S; LARGEN P; ODONNELL M; REAVELEY D; CATTELL V;
Indirizzi:
ST MARYS HOSP,SCH MED,DEPT HISTOPATHOL,NORFOLK PL LONDON W2 1PG ENGLAND UNIV LONDON IMPERIAL COLL SCI TECHNOL & MED,ST MARYS HOSP,SCH MED,DEPT HISTOPATHOL LONDON W2 ENGLAND CHARING CROSS & WESTMINSTER MED SCH,DEPT CHEM PATHOL LONDON W6 ENGLAND
Titolo Testata:
American journal of physiology. Renal, fluid and electrolyte physiology
fascicolo: 4, volume: 36, anno: 1994,
pagine: 60000646 - 60000653
SICI:
0363-6127(1994)36:4<60000646:AMIEG->2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
NECROSIS-FACTOR-ALPHA; IMMUNE-COMPLEX GLOMERULONEPHRITIS; GLOMERULI SYNTHESIZE NITRITE; RENAL MESANGIAL CELLS; RAT; MACROPHAGES; EXPRESSION; INHIBITION; MECHANISM; CULTURE;
Keywords:
L-ORNITHINE; MESANGIAL CELL;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
51
Recensione:
Indirizzi per estratti:
Citazione:
H.T. Cook et al., "ARGININE METABOLISM IN EXPERIMENTAL GLOMERULONEPHRITIS - INTERACTION BETWEEN NITRIC-OXIDE SYNTHASE AND ARGINASE", American journal of physiology. Renal, fluid and electrolyte physiology, 36(4), 1994, pp. 60000646-60000653

Abstract

L-Arginine is metabolized by two pathways: 1) by nitric oxide synthase (NOS) to nitric oxide (NO) and 2) by arginase forming urea and L-ornithine. Inflammatory responses may involve a balance between the pathways, as NO is cytotoxic and vasodilatory and L-ornithine is a promoterof cell proliferation and matrix synthesis. In experimental glomerulonephritis we have previously shown that NOS is activated in nephritic glomeruli. We have now examined both pathways of L-arginine metabolismto study competition for L-arginine, temporal variation, and the sources of NOS and arginase. Acute in situ glomerulonephritis was induced in rats, and glomeruli were studied at 1, 4, and 7 days. Both NOS and arginase activities were present. There was temporal variation: NOS activity was highest on day 2 and arginase activity on day 4; both declined by day 7. Competition between the pathways was demonstrated by increased urea synthesis in the presence of N-G-monomethyl-L-arginine, aninhibitor of NOS. Measurement of NOS and arginase activities in macrophages isolated from nephritic glomeruli showed that these cells were a major source of glomerular NOS but not arginase activity. In contrast, high arginase activity but low NO production was identified in cultured rat glomerular mesangial cells. These studies show differential temporal variation in expression of NOS and arginase pathways of arginine metabolism in experimental glomerulonephritis. We have found two factors that may contribute to this: 1) competition for substrate L-arginine between the two pathways and 2) different cellular sources. We hypothesize that the balance between these pathways is a mechanism regulating injury, hemodynamics, and mesangial cell proliferation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 19:42:15