L-arginine-NO pathway in hemodialysis

Citation
P. Gomez-fernandez et al., L-arginine-NO pathway in hemodialysis, NEFROLOGIA, 20(3), 2000, pp. 262-268
Citations number
29
Categorie Soggetti
Urology & Nephrology
Journal title
NEFROLOGIA
ISSN journal
02116995 → ACNP
Volume
20
Issue
3
Year of publication
2000
Pages
262 - 268
Database
ISI
SICI code
0211-6995(200005/06)20:3<262:LPIH>2.0.ZU;2-2
Abstract
Nitric oxide (NO) is derived from the metabolism of the amino acid L-argini ne by NO synthase (NOS). One of the forms of NOS (i-NOS) can be induced by cytokines, bradykinin and endotoxin. During hemodialysis (HD), blood-dialys is membrane interaction can induce production of these mediators. HD can al so induce changes of asymmetrical dimethylarginine (ADA), a potent inhibito r of NOS. The aim of this study was to investigate the effect of HD, using cuprophane (C, polyacrilonytrile (PAN) and special polyacrylonitrile (SPAN) membranes , on cellular NOS activity: and changes of plasma tumor necrosis Factor (TN F-alpha) bradykinin, ADA and nitrate concentration. Before HD, cellular i-NOS activity was similar with the three membranes. Cu prophane HD induced a significant increase in i-NOS activity From 31 +/- 10 to 48 +/- 12 fmol(-1) 10(6) cells (p < 0.05). No changes were found in PAN and SPAN HD. The TNF-alpha values increased significantly during HD with C (56 +/- 6 vs 47 +/- 5 pg/ml, p < 0.05). No changes of bradykinin concentra tion were found during HD. A significant decrease of ADA and nitrate levels nas observed during HD with three membranes. No significant correlation wa s found between percentage increase in i-NOS activity and the changes in ot her parameters. These Findings suggest that HD with bioincompatible membranes can induce ac tivation of cellular i-NOS.