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Titolo:
L-ARGININE DEPLETION INHIBITS GLOMERULAR NITRIC-OXIDE SYNTHESIS AND EXACERBATES RAT NEPHROTOXIC NEPHRITIS
Autore:
WADDINGTON S; COOK HT; REAVELEY D; JANSEN A; CATTELL V;
Indirizzi:
UNIV LONDON IMPERIAL COLL SCI TECHNOL & MED,SCH MED,DEPT HISTOPATHOL,ST MARYS HOSP,NORFOLK PL LONDON W2 1PG ENGLAND UNIV LONDON IMPERIAL COLL SCI TECHNOL & MED,SCH MED,DEPT HISTOPATHOL,ST MARYS HOSP LONDON W2 1PG ENGLAND CHARING CROSS & WESTMINSTER MED SCH,DEPT CHEM PATHOL LONDON ENGLAND
Titolo Testata:
Kidney international
fascicolo: 4, volume: 49, anno: 1996,
pagine: 1090 - 1096
SICI:
0085-2538(1996)49:4<1090:LDIGNS>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
MESANGIAL CELLS; INJURY; GLOMERULONEPHRITIS; THROMBOSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
27
Recensione:
Indirizzi per estratti:
Citazione:
S. Waddington et al., "L-ARGININE DEPLETION INHIBITS GLOMERULAR NITRIC-OXIDE SYNTHESIS AND EXACERBATES RAT NEPHROTOXIC NEPHRITIS", Kidney international, 49(4), 1996, pp. 1090-1096

Abstract

Nitric oxide (NO) synthesis is induced in glomeruli in glomerulonephritis; its role in the pathogenesis of glomerular injury is unknown. Interpretation of its role using the currently available analogues of L-arginine as in vivo inhibitors of NO is complicated by their lack of specificity for inducible NO synthase (iNOS). As NO synthesis by iNOS depends on extracellular L-arginine, we have here examined effects of L-arginine depletion on glomerular NO synthesis and the course of accelerated nephrotoxic nephritis (NTN). Arginase, which converts L-arginine to urea and L-ornithine, was used to achieve L-arginine depletion. Asingle dose of i.v. arginase produced complete depletion of plasma arginine for four hours. Two forms of NTN were induced in preimmunised rats by nephrotoxic globulin: (1) the systemic form of the model by intravenous nephrotoxic globulin; or (2) the unilateral form of model by left kidney perfusion with nephrotoxic globulin, which avoids the complications of systemic administration of nephrotoxic globulin. Arginasereduced plasma arginine levels and the synthesis of nitrite (the stable end-product of NO) by NTN glomeruli (95% inhibition). Proteinuria was exacerbated. There was no effect on early (24 hr) leukocyte infiltration. In the systemic form of the model arginine depletion by i.v. arginase increased glomerular thrombosis at 24 hours, and the severity of histological changes at four days, accompanied by systemic hypertension. In the unilateral form of the model, where i.v. arginase did not induce hypertension, there was no increase in thrombosis or histological severity of nephritis. These results show that arginine depletion, which inhibits glomerular NO synthesis in NTN, leads to increased proteinuria. Where injury is severe, or accompanied by systemic hypertension, the disease is further exacerbated by glomerular thrombosis. Theseresults suggest that NO has an important role in limiting acute glomerular injury.

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Documento generato il 01/12/20 alle ore 16:17:52