Kivonat:
1. The role of nitric oxide synthases (NOS) and the nitric oxide
(NO) substrate l-arginine in renal ischaemia-reperfusion (I/R)
has been studied extensively. However, the results reported are
often controversial. In the present study, we examined the
effects of the neuronal (n) NOS inhibitor 7-nitroindazole (7-NI)
and l-arginine administration on renal I/R injury and the renal
NO system in rats. 2. Following7 days pretreatment with 7-NI (50
mg/kg per day), L-arginine (2 g/kg per day) or vehicle
(dimethylsulphoxide : sesame oil, I : 9), the left renal
vascular pedicles were clamped for 50 min in male Sprague-Dawley
rats and kidneys were removed 24 h after reperfusion (n =
7/group). 3. Neither 7-NI nor l-arginine had any effect on
parameters of renal function, the grade of tissue injury or the
number of terminal deoxyribonucleotidyl transferase-mediated
dUTP-digoxigenin nick end-labelling (TUNEL)-positive tubular
cells compared with vehicle-treated rats. 7-Nitroindazole
decreased nNOS mRNA expression anti inducible (i) NOS protein
levels, but had no effect on endothelial NOS expression. l-
Arginine supplementation increased mRNA expression of all NOS
isoforms, but only increased protein expression of iNOS. 4. The
results of the present study demonstrate that selective
inhibition of nNOS has no effect (in renal injury, indicating
that nNOS does not play a central role in the pathophysiology of
renal I/R. In addition, although i,l-arginine has no effect on
renal I/R injury in the model used in the present study, its
administration increases the mRNA expression of NOS isoforms.