作者: Takeshi F. Andoh , Michael P. Gardner , William M. Bennett
DOI: 10.1097/00007890-199711150-00002
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摘要: Background L-Arginine (L-Arg), the substrate for nitric oxide (NO) synthase producing NO, and NO inhibitor, N-nitro-L-arginine-methyl ester (L-NAME), have both been shown to modify acute cyclosporine (CsA)-induced intrarenal vasoconstriction. However, mechanism of chronic CsA nephrotoxicity characterized by progressive tubulointerstitial fibrosis (TIF) remains unclear. Thus, we examined pathogenetic role in a rat model nephropathy. Methods Rats were given vehicle, (7.5 mg/kg), + L-Arg (1.7 g/kg), D-arginine L-NAME (3.5 mg/kg) 28 days on low-salt diet. production, glomerular filtration rate (GFR), blood urine chemistry, histology assessed. Results treatment significantly enhanced biosynthesis protected animals from impaired GFR development TIF induced CsA, whereas did not. In contrast, strikingly reduced urinary worsened compared alone group, not change renal function vehicle group. Conclusions Chronic can be aggravated blockade ameliorated enhancement, suggesting that has an important